Curcumin (turmeric) is the main ingredient of the Chinese herbal turmeric rhizome, used to treat tumors, diabetes, inflammation, neurodegenerative diseases, cardiovascular diseases, metabolic syndrome, and liver diseases. The antitumor effects of curcumin have received even more attention. One of the main mechanisms of the antitumor effects includes inhibition of tumor invasion and migration, induction of tumor cell apoptosis, and inhibition of various cell signaling pathways. It has been found that the antitumor biological activity of curcumin in the body is associated with epigenetic mechanisms. That also implies that curcumin may act as a potential epigenetic modulator to influence the development of tumor diseases. The immune system plays an essential role in the development of tumorigenesis. Tumor immunotherapy is currently one of the most promising research directions in the field of tumor therapy. Curcumin has been found to have significant regulatory effects on tumor immunity and is expected to be a novel adjuvant for tumor immunity. This paper summarizes the antitumor effects of curcumin from four aspects: molecular and epigenetic mechanisms of curcumin against a tumor, mechanisms of curcumin modulation of tumor immunotherapy, reversal of chemotherapy resistance, and a novel drug delivery system of curcumin, which provide new directions for the development of new antitumor drugs.

More research has been done on the correlation between exercise and cancer, which has revealed several ways that physical activity decreases the risk of developing the disease. The developing function of lncRNAs as an important molecular link between exercise and cancer suppression is the main topic of this review. According to recent research, regular physical exercise also alters the expression levels of several lncRNAs, which are generally elevated in cancer. A complex network of interactions that may provide protective effects against carcinogenesis is suggested by the contribution of these lncRNAs in various cellular processes, such as epigenetic alterations, proliferation, and apoptosis regulation. We offer a comprehensive summary of the existing information regarding specific lncRNAs that are influenced by physical activity and could potentially impact cancer-related processes. We also go over the difficulties in interpreting these alterations, taking into account the fact that several lncRNAs have a dual function in promoting and preventing cancer in various physiological settings. To understand the complex impacts of exercise-induced lncRNA regulation in cancer biology, more study is required. The critique strongly highlights the possibility of lncRNAs serving as both indicators and treatment prospects for cancer-preventive strategies.

Myocardial ischemia/reperfusion (I/R) injury is a common pathophysiological change after myocardial reperfusion therapy. Recent research confirmed that long non-coding RNA (IncRNAs) played an important role in many cardiovascular diseases. This study was carried out to explore the role of lncRNA XR008038 in the I/R progression.

GSE103731 database was downloaded from NCBI Gene Expression Omnibus to analyze the differently expressed lncRNAs. Cell viability was determined by CCK-8 assay. Cell apoptosis was detected by flow cytometry and TUNEL staining. Northern blot and qRT-PCR was carried out to detect the XR008038 levels. The mitochondrial membrane potential was assessed by JC-1 staining. Western blot was conducted to measure the expression of apoptosis related proteins. RNA pull down and RIP assay was carried out to explore the relationship between XR008038 and galectin-3.

The results showed that XR008038 was up-regulated in the H/R treated H9c2 cells and the myocardial tissues of the I/R rats. XR008038 silencing promoted the cell growth and mitochondrial membrane potential, inhibited the cell apoptosis of the H/R treated H9c2 cells. Additionally, the MDA content was decreased and SOD activity was enhanced in the H/R treated H9c2 cells and the myocardial tissues of the I/R rats after XR008038 knockdown. XR008038 interacted with galectin-3 and further regulated the mRNA stability of galectin-3. Galectin-3 overexpression neutralized the role of si-XR008038 in the H/R treated H9c2 cells.

In conclusion, XR008038 promoted the oxidative damage in I/R progression through regulating the galectin-3 levels.

Increasing evidence suggests that non-coding small RNAs (miRNAs) carried by exosomes (EXOs) play important roles in the development and treatment of polycystic ovary syndrome (PCOS). In this study, we demonstrate that PCOS mouse serum-derived EXOs promote granulosa cells (GCs) ferroptosis, and induce the occurrence of a PCOS-like phenotype in vivo. Notably, EXO miRNA sequencing combined with in vitro gain- and loss-of-function assays revealed that miR-128-3p, which is absent in the serum-derived EXOs of mice with PCOS, regulates lipid peroxidation and GC sensitivity to ferroptosis inducers. Mechanistically, overexpression of CSF1, a direct target of miR-128-3p, reversed the anti-ferroptotic effect of miR-128-3p. Conversely, ferroptosis induction was mitigated in CSF1-downregulated GCs. Furthermore, we demonstrated that miR-128-3p inhibition activates the p38/JNK pathway via CSF1, leading to NRF2-mediated down-regulation of SLC7A11 transcription, which triggers GC iron overload. Moreover, intrathecal miR-128-3p AgomiR injection into mouse ovaries ameliorated PCOS-like characteristics and restored fertility in letrozole-induced mice. The study reveals the pathological mechanisms of PCOS based on circulating EXOs and provides the first evidence of the roles of miR-128-3p and CSF1 in ovarian GCs. This discovery is expected to provide promising therapeutic targets for the treatment of PCOS.

This study aims to discover the role of lncRNA MIR17HG, referred to as MIR17HG, in cisplatin resistance for cholangiocarcinoma (CCA).

QRT-PCR was conducted to measure the expression of MIR17HG in cisplatin-resistant/sensitive CCA cells and clinical CCA specimens. Log-rank test was used to analyze the survival curve. Cck8-assay and flow cytometry were employed to detect the sensitivity of CCA cells to cisplatin and the apoptosis rate following different treatments, respectively. The next-generation sequencing was carried out to get gene transcripts after silencing MIR17HG in HCCC-9810 cells. The LncBase database was used to predict the target miRNA of MIR17HG, and MS2 RIP assay and dual luciferase assay were conducted to confirm their binding. MiRwalk database and the RNA sequencing data were utilized to screen the key genes regulated by MIR17HG/miR-138-5p axis and a dual luciferase assay was performed to confirm the binding site of miR-138-5p with AKAP9. Immunoblotting was further employed to give assistant evidence. Rescue experiments were performed to observe the function of miR-138-5p and AKAP9 in MIR17HG-induced cisplatin resistance.

MIR17HG overexpression predicts cisplatin resistance and poor prognosis in CCA. MIR17HG could bind with miR-138-5p to release AKAP9, thereby inhibiting cisplatin-induced apoptosis and promoting cisplatin resistance in CCA. MIR17HG silencing in CCA cells leads to expression alteration of genes, which are enriched in platinum resistance-related pathways.

LncRNA MIR17HG regulates platinum resistance-associated genes and promotes cisplatin resistance partially via the miR-138-5p/AKAP9 axis by inhibiting cisplatin-induced apoptosis in CCA.

Long noncoding RNA (lncRNA) plays a critical role in cancer cell proliferation, invasion, metastasis, and chemoresistance. The current study introduces novel lncRNAs in colorectal cancer (CRC) through bioinformatics analysis. GSE134834 CRC-related microarray of Gene Expression Omnibus (GEO) was analyzed to identify differentially expressed genes (DEGs) in CRC samples against normal samples. Analysis revealed 6763 DEGs (p < 0.05 and |log fold change (FC)| ≥ 0.5) that include differentially expressed mRNA (DEmRNA) and differentially expressed long noncoding RNA (DElncRNA). Novel lncRNAs were identified, and to better understand the biological function of the identified lncRNAs, gene modules were constructed using weighted gene coexpression network analysis (WGCNA), and finally, two modules for lncRNAs were obtained. The coexpression modules with these lncRNAs were subjected to enrichment analysis in FunRich software to predict their functions through their coexpressed genes. Gene ontology results of modules related to novel lncRNA revealed they significantly enriched the cellular pathways regulation in cancer. The protein-protein interaction (PPI) network of novel lncRNAs-related modules was constructed using Search Tool for the Retrieval of Interacting Genes (STRING) and visualized using the Cytoscape software. Hub genes were screened from the PPI network by the CytoHubba plug-in of Cytoscape. The hub genes were MRTO4, CDK1, CDC20, RPF2, NOP58, NIFK, GTPBP4, BUB1, BUB1B, and BOP1 for the lightpink4 module and BYSL, RPS23 (ribosomal protein S23), RSL1D1 (ribosomal L1 domain containing 1), NAT10, NOP14, GNL2, MRPS12, NOL6 (nucleolar protein 6), IMP4, and RRP12 (ribosomal RNA processing 12 homolog) for the pink module. The expression levels of the top DEmRNA and module hub genes in CRC were validated using the Gene Expression Profiling Interactive Analysis (GEPIA) database. Generally, our findings offer crucial insight into the hub genes and novel lncRNAs in the development of CRC by bioinformatics analysis, information that may prove useful in the identification of new biomarkers and treatment targets in CRC; however, more experimental investigation is required to validate the findings of the present study.

Long non-coding RNAs (lncRNAs) play a pivotal role in regulating gene expression and are critically involved in the progression of malignant brain tumors, including glioblastoma, medulloblastoma, and meningioma. These lncRNAs interact with microRNAs (miRNAs), proteins, and DNA, influencing key processes such as cell proliferation, migration, and invasion. This review highlights the multifaceted impact of lncRNA dysregulation on tumor progression and underscores their potential as therapeutic targets to enhance the efficacy of chemotherapy, radiotherapy, and immunotherapy. The insights provided offer new directions for advancing basic research and clinical applications in malignant brain tumors.

Epithelial ovarian cancer is responsible for the majority of ovarian malignancies, and its highly invasive nature and chemoresistant development have been major obstacles to treating patients with mainstream treatments. In recent decades, the significance of microRNAs (miRNAs), circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and competing endogenous RNAs (ceRNAs) has been highlighted in ovarian cancer development. This hidden language between these RNAs has led to the discovery of enormous regulatory networks in ovarian cancer cells that substantially affect gene expression. Aside from providing ample opportunities for targeted therapies, circRNA- and lncRNA-mediated ceRNA network components provide invaluable biomarkers. The current study provides a comprehensive and up-to-date review of the recent findings on the significance of these ceRNA networks in the hallmarks of ovarian cancer oncogenesis, treatment, diagnosis, and prognosis. Also, it provides the authorship with future perspectives in the era of single-cell RNA sequencing and personalized medicine.

Colorectal cancer (CRC) ranks among the top three cancers globally in both incidence and mortality, posing a significant public health challenge. Most CRC cases are diagnosed at intermediate to advanced stages, and reliable biomarkers for early detection are lacking. Long non-coding RNAs (lncRNAs) have been implicated in various cancers, including CRC, playing key roles in tumor development, progression, and prognosis.

A comprehensive search of the PubMed database was conducted to identify relevant studies on the early diagnosis of CRC. Bioinformatics analysis was performed to explore lncRNA-mRNA networks, leading to the identification of five potential blood biomarkers. Expression analysis was carried out using the GEPIA and GEO online databases, focusing on MYC and STAT3. Differential expression between normal and CRC tissues was assessed, followed by Receiver Operating Characteristic (ROC) analysis to evaluate the diagnostic potential of these markers. Quantitative Real-Time PCR (qRT-PCR) was performed to validate MYC and STAT3 expression levels, and findings were further confirmed using the Human Protein Atlas (HPA) database.

Database analysis revealed significant differential expression of MYC and STAT3 between normal and CRC tissues. ROC analysis demonstrated the diagnostic potential of these markers. qRT-PCR validation confirmed the differential expression patterns observed in the databases. Validation through the HPA database further supported these findings, confirming the potential of MYC and STAT3 as diagnostic biomarkers for CRC.

Our results suggest that MYC and STAT3 are promising diagnostic biomarkers for CRC, offering new insights into its pathophysiology and potential for targeted therapies.

Colorectal cancer (CRC) is an aggressive malignancy among malignant tumours, with a high incidence globally. LINC01614, a long non-coding RNA, has been identified as an essential regulator in multiple cancer types. However, its biological functions and underlying molecular mechanisms in CRC remain largely unknown.

In this study, we employed RT-qPCR to assess the expression levels of LINC01614 in CRC samples. In vitro, glucose metabolism experiments were conducted to evaluate glucose metabolism in cells. The binding relationship between miR-4443, PFKFB3, and LINC01614 was confirmed through fluorescence reporter gene detection. The subcellular localization of LINC01614 in CRC cells was determined using FISH and subcellular fractionation experiments. Additionally, a mouse subcutaneous tumor model was established for in vivo experiments.

Our findings reveal that LINC01614 is upregulated in CRC tissues. Silencing of LINC01614 suppresses the malignant behaviors of CRC cells, including cell proliferation, invasion, migration, and aerobic glycolysis. Furthermore, we discovered that LINC01614 promotes the expression of PFKFB3. Additional experiments demonstrated that LINC01614 binds to miR-4443, leading to the upregulation of PFKFB3 expression. Further experiments confirmed that the LINC01614/miR-4443/PFKFB3 axis promotes CRC cell malignancy by enhancing aerobic glycolysis. Additionally, we found that STAT1 promotes the transcription of LINC01614.

These findings uncover a novel regulatory pathway wherein STAT1-induced LINC01614 enhances PFKFB3 expression by sponging miR-4443, thereby accelerating CRC development. This understanding may lead to novel therapeutic strategies for CRC treatment.

Long intergenic noncoding RNAs (lincRNAs) have a variety of properties that differ from those of messenger RNAs (mRNAs) encoding proteins. Long intergenic nonprotein coding RNA 667 (LINC00667) is a non-coding transcript located on chromosome 18p11.31. Recently, many studies have found that LINC00667 can enhance the progression of various cancers and play a key part in a lot of diseases, such as tumorigenesis. Therefore, LINC00667 can be recognized as a potential biomarker and therapeutic target. So, we reviewed the biological functions, relevant mechanisms, as well as clinical significance of LINC00667 in several human cancers in detail.

The expression level of exosomal long non-coding RNAs (lncRNAs) can be relevant for clinical diagnostic approaches. The object of our study was to evaluate the differential expression of lncRNAs colon cancer associated transcript 1 (CCAT1) and X-inactive specific transcript (XIST) in plasma exosomes of colorectal cancer (CRC) patients and investigate their potential as clinical biomarkers. In a case-control study, 62 CRC patients and 62 healthy persons were studied. Plasma exosomes were isolated by a centrifugation approach and were characterized by microscopy and western blotting. After RNA extraction and cDNA synthesis, using real-time PCR technique, the relative expression of lncRNAs was evaluated. The expression levels of lncRNA CCAT1, but not XIST, were meaningfully increased in the plasma-derived exosomes of CRC patients compared to non-cancer individuals (p= 0.001, 0.083 respectively). Further analyses revealed that the expression levels of exosomal lncRNA CCAT1 were associated with the lymphovascular invasion and tumor differentiation (p<0.05). ROC curve analysis documented a diagnostic power for lncRNA CCAT1 in CRC with a sensitivity of 79% and a specificity of 80% with an optimal cutoff point 6.5, with an area under curve (AUC)=86% and p<0.0001. Also, lncRNA XIST revealed a sensitivity of 62% and a specificity of 61% with a cutoff point 2.4, with an AUC=65%. Our findings indicated the potential of plasma-derived exosomal lncRNA CCAT1 as a non-invasive clinical indicator for the diagnosis of CRC patients.

Long noncoding RNAs (lncRNAs) have emerged as critical regulators in the development of colorectal cancer (CRC). Previous studies indicate that lncRNA FEZF1-AS1 is highly expressed in CRC, but its role in modulating CRC via the P53 signaling pathway remains unclear. In this study, we found that FEZF1-AS1 promotes the growth of the CRC cell line (HCT116) and drives epithelial-mesenchymal transition (EMT) through the P53 signaling pathway. Our data showed that FEZF1-AS1 expression is significantly upregulated in HCT116, and elevated levels of FEZF1-AS1 are associated with poor prognosis in patients with CRC. In addition, the knockdown of FEZF1-AS1 markedly inhibited the proliferation of HCT116 by inducing cell cycle arrest. Knockdown of FEZF1-AS1 depletion also led to apoptosis in CRC cells by suppressing the P53 signaling pathway and EMT, thereby reducing their viability, proliferation, migration, and invasion. In summary, this study confirmed that FEZF1-AS1 regulates the growth of junction HCT116 through P53 signaling pathway and inhibiting EMT, providing new insights for the potential therapeutic strategies against CRC.

Triple-negative breast cancer (TNBC) seriously threatens women's health, and long noncoding RNAs (lncRNAs) are emerging as critical regulators of gene expression and play fundamental roles in TNBC. This study aimed to identify lncRNAs that represent effective targets for the early diagnosis or treatment of TNBC. Here, we utilized the TCGA database to analyze differentially expressed genes, and survival analysis and ROC curve analysis were also performed. Notably, we identified a novel lncRNA, AC112721.1, that is significantly overexpressed in TNBC and is associated with poor overall survival in TNBC patients. Loss- and gain-of-function experiments revealed that AC112721.1 significantly promoted cell proliferation and migration, suppressed cell apoptosis in vitro and inhibited tumorigenesis in vivo. Further study of the mechanisms underlying these effects revealed that AC112721.1 regulates the Ras pathway by directly binding to THBS1 protein and functions as a ceRNA by sponging miR-491-5p to increase the expression of C2CD2L, thereby influencing the progression of TNBC. Our findings indicate that AC112721.1 may represent a new biomarker for evaluating TNBC prognosis and treating TNBC.

Cervical squamous cell carcinoma (CSCC) has a poor prognosis due to persistent HPV infection. LncRNA TPRG1-AS1 is linked to regulating the development of many cancers, so the regulatory mechanism and prognostic value of TPRG1-AS1 in CSCC were explored.

138 patients with cervical cancer were included. TPRG1-AS1 expression and miR-590-3p were analyzed by qRT-PCR. The association between TPRG1-AS1 and clinicopathological features was investigated. Independent prognostic factors of CSCC were analyzed by multifactorial Cox regression. Patient survival was analyzed using Kaplan-Meier plotter curves. CCK-8 was employed to evaluate the proliferative capacity of the cells. Transwell assays were performed to evaluate the effects of TPRG1-AS1 and miR-590-3p on cell migration and invasion performance, and the target of both was reported by DLR assay.

TPRG1-AS1 levels were ascended in CSCC, and miR-590-3p levels were reduced. TPRG1-AS1 and miR-590-3p target binding and expression correlated negatively. Knockdown of TPRG1-AS1 expression could facilitate high miR-590-3p expression, which reduced cell proliferation, migration, and invasion ability. TPRG1-AS1 is an independent prognostic factor.

TPRG1-AS1 has potential as a prognostic marker for CSCC. Silencing the expression of TPRG1-AS1 could contribute to the high miR-590-3p expression thereby slowing down the progression of CSCC.

Gastrointestinal (GI) cancers, such as gastric cancer, hepatocellular carcinoma, colorectal cancer, and esophageal cancer, pose a significant medical and economic burden globally, accounting for the majority of new cancer cases and deaths each year. A lack of knowledge about the molecular mechanisms of GI cancers is reflected in the low efficacy of treatment for individuals with late stage and recurring illness. Understanding the molecular pathways that promote the growth of GI cancers may open doors for their therapy. Numerous long non-coding RNAs (lncRNAs) that are produced differently in normal and malignant tissues have been discovered by genome-wide techniques. The role of lncRNAs in the diagnosis, proliferation, metastasis, and drug resistance of different GI cancers has been investigated in recent research. LncRNAs may affect transcription, epigenetic modifications, protein/RNA stability, translation, and post-translational modifications via their interactions with DNA, RNAs, and proteins. Also, by functioning as competing endogenous RNAs (ceRNAs), they control the synthesis of certain microRNAs (miRNAs), which in turn modify the downstream target molecules of these miRNAs. Based on recent studies, lncRNAs in particular, CRNDE and HOTAIR, sponge different miRNAs and their downstream genes, which in turn regulate GI cancers development, including cell proliferation, invasion, migration, and chemoresistance. In this comprehensive review, we present an overview of the biological roles of CRNDE and HOTAIR and their associated mechanisms, miRNAs/mRNA pathways, in various GI cancers, encompassing colorectal cancer, hepatocellular carcinoma, esophageal cancer, and gastric cancer.

Colorectal cancer (CRC) is one of the leading causes of cancer-related mortality. LncRNA NORAD is frequently upregulated and positively associated with various cancer progressions. We discovered NORAD was significantly upregulated in CRC tissues and cells. NORAD sponged miR-106a-5p to form a ceRNA complex. MiR-106a-5p was remarkedly downregulated in CRC tumors and cells. Silencing NORAD or overexpression of miR-106a-5p effectively increased cisplatin sensitivity. In the established cisplatin resistant cell line, NORAD was upregulated and miR-106a-5p was downregulated. Furthermore, we disclosed miR-106a-5p directly targeted 3'UTR of CCND1, which is an important cell cycle regulator and is frequently overexpressed in human cancers. Rescue experiments showed restoration of CCND1 in miR-106a-5p-overexpressing CRC cells successfully recovered cisplatin resistance. Finally, restoration of miR-106a-5p in NORAD-overexpressing CRC cells re-sensitized cisplatin resistance by targeting CCND1. Summarily, this study uncovered a NORAD-promoted cisplatin resistance through modulating the miR-106a-5p-CCND1 axis, contributing to developing novel therapy for treating chemoresistant CRC.

Lenvatinib is a multitargeted tyrosine kinase inhibitor (TKI) used in the upfront and refractory settings for metastatic renal cell carcinoma (mRCC). However, there are limited data on the efficacy of subsequent TKI therapies after lenvatinib. We investigated the activity of TKI therapies after lenvatinib in patients with mRCC.

We conducted a retrospective analysis of data from the International Metastatic RCC Database Consortium (IMDC). Patients who received post-lenvatinib treatment were divided into two cohorts: a second-line cohort after first-line lenvatinib; and a third-line cohort after second-line lenvatinib. The primary endpoint was the objective response rate (ORR). Secondary endpoints included the time to treatment failure (TTF).

Of the 168 patients included, 122 (73%) had clear-cell histology. In the second-line cohort (n = 20), all patients received first-line pembrolizumab + lenvatinib. The ORR was 50% and median TTF was 19.7 mo for first-line treatment. Median follow-up from initiation of second-line treatment was 4.9 mo. The ORR to second-line treatment was 5% (95% confidence interval [CI] 0.2-25%) and median TTF was 5.8 mo (95% CI 1.9-14.9). In the third-line cohort (n = 34), most patients received second-line everolimus + lenvatinib (97%). The ORR was 31% and median TTF was 9.2 mo for second-line therapy. Median follow-up from initiation of third-line treatment was 14.9 mo. The ORR to third-line treatment was 12% (95% CI 3.3-27%) and median TTF was 2.8 mo (95% CI 1.9-7.4).

Our data demonstrate modest activity of TKI-based therapy after exposure to lenvatinib. The results highlight the need for better treatment options for patients who experience progression on lenvatinib-based therapies.

Lenvatinib is a type of drug called a tyrosine kinase inhibitor (TKI). It is used to treat metastatic kidney cancer either when first diagnosed or after progression on a previous treatment. There is limited information on how patients respond to a different TKI after receiving lenvatinib. Our results show that other TKIs have modest clinical activity after patients have received lenvatinib.

Exploring effect biomarkers that monitor tumor progression and predict the prognosis could benefit the clinical management of bladder cancer and improve the postoperative life of patients. This study aimed to estimate the function of long non-coding (lnc)RNA RHPN1-AS1 (RHPN1-AS1) in bladder cancer and the potential molecular mechanism.

The expression of RHPN1-AS1 was evaluated in bladder cancer tissues from 115 patients and cells by polymerase chain reaction. The clinical significance of RHPN1-AS1 was assessed and its effect was also estimated in cell proliferation, migration, and invasion. The underlying molecular mechanism was explored by the dual-luciferase reporter assay.

The expression of RHPN1-AS1 was 2.91-fold elevated in bladder cancer, which showed a close correlation with advanced tumor node metastasis stage (P = 0.013) and the presence of lymph node metastasis (P = 0.018). RHPN1-AS1 also served as a poor prognostic indicator (hazard ratio = 2.563) for bladder cancer. The knockdown of RHPN1-AS1 significantly suppressed the proliferation and metastasis ability of bladder cancer cells. Moreover, miR-485-5p was found to mediate the function of RHPN1-AS1 in bladder cancer, which was considered the underlying regulatory mechanism.

RHPN1-AS1 serves as a prognostic biomarker and tumor promoter in bladder cancer via modulating miR-485-5p, which might be a reliable target of bladder cancer therapy.

Infectious bursal disease virus (IBDV) causes immunosuppression and high mortality in young chickens. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are important regulators during viral infection. However, detailed the regulatory mechanisms of lncRNA-miRNA-mRNA have not yet been described in IBDV infection. Here, we analysed the role of lncRNA53557/gga-miR-3530-5p/STAT1 axis in very virulent IBDV (vvIBDV) infection. Evidently upregulated expression of lncRNA53557 was observed in bursa of Fabricius and DT40 cells. Meanwhile, overexpression of lncRNA53557 promoted STAT1 expression and inhibited vvIBDV replication and vice versa, indicating that the upregulation of lncRNA53557 was part of the host antiviral defence. The subcellular fractionation assay confirmed that lncRNA53557 can be localized in the cytoplasm. Further, dual-luciferase reporter, RNA pulldown, FISH and RT-qPCR assays revealed that lncRNA53557 were directly bound to gga-miR-3530-5p and had a negative regulatory relationship between them. Subsequent mechanistic analysis showed that lncRNA53557 acted as a competing endogenous RNA (ceRNA) of gga-miR-3530-5p to relieve the repressive effect of gga-miR-3530-5p on its target STAT1, as well as Mx1, OASL, and ISG15, thereby suppressing vvIBDV replication. The study reveals that a network of enriched lncRNAs and lncRNA-associated ceRNA is involved in the regulation of IBDV infection, offering new insight into the mechanisms underlying IBDV-host interaction.

Hepatocellular carcinoma (HCC) is a malignancy characterized by a high fatality rate. Increasing evidence indicating that long non-coding RNAs (lncRNAs) play a regulatory role in hepatocellular carcinoma (HCC). Among them, the correlation between LINC02298 and HCC remains unknown. The expression and subcellular localization of LINC02298 in HCC tissues and cell lines were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Furthermore, the correlation between the expression of LINC02298 and clinicopathological features of HCC patients was analyzed. The regulatory effects of LINC02298 in HCC were investigated using colony formation, cell count Kit-8(CCK8), Transwell, EDU, cell cycle and apoptosis analysis. In addition, the expression of EMT-related proteins were detected by western blotting. Dual-luciferase reporter, RT-qPCR and rescue assays were employed to validate the involvement of the LINC02298/miR-28-5p/CCDC6 axis in the progression of HCC. The up-regulation of LINC02298 was observed in hepatocellular carcinoma (HCC) tissues and cells, and it was found to be correlated with a negative prognosis in patients with HCC. Overexpression of LINC02298 enhanced the proliferation, migration, invasion, and induction of Epithelial-Mesenchymal Transition (EMT) while suppressing apoptosis in HCC cells. LINC02298 bind to miR-28-5p to regulate the expression of CCDC6. Inhibition of miR-28-5p saved the inhibitory effect of shLINC02298, and knockdown of CCDC6 also saved the inhibitory effect of miR-28-5p on HCC in vitro and in vivo. LINC02298 regulates the expression of CCDC6 by sponging of miR-28-5p, thereby facilitating the the malignancy and EMT of HCC.

Colorectal cancer (CRC) is a widespread cancerous disease with an unfavorable prognosis. MIR210HG appears to have a significant connection with the development of CRC, but the precise regulatory mechanism remains obscure.

Quantitative real-time polymerase chain reaction was utilized to determine expression quantities of MIR210HG and miR-1226-3p. The proliferative capacity of CRC cells was measured by cell counting kit-8. The apoptosis rate of cells was examined using flow cytometry. The invasive capability was assessed through the transwell experiment. The targeted regulation of MIR210HG and miR-1226-3p was validated through dual-luciferase reporter gene experiments.

In carcinoma tissues and blood serum of colorectal cancer patients and cell lines, MIR210HG expression was upregulated, while the miR-1226-3p expression was downregulated. MIR210HG had a diagnostic and prognostic value for CRC patients. MIR210HG may target and regulate miR-1226-3p. MIR210HG may have the capacity to augment the vitality and invasion of CRC cells and suppress cell apoptosis, and this influence is counteracted by miR-1226-3p.

lncRNA MIR210HG accelerated the progression of colorectal cancer by controlling miR-1226-3p. lncRNA MIR210HG/miR1226-3p may potentially serve as therapeutic targets for addressing colorectal cancer.

Non-alcoholic fatty liver disease (NAFLD) poses a global health challenge. While pyroptosis is implicated in various diseases, its specific involvement in NAFLD remains unclear. Thus, our study aims to elucidate the role and mechanisms of pyroptosis in NAFLD. Utilizing data from the Gene Expression Omnibus (GEO) database, we analyzed the expression levels of pyroptosis-related genes (PRGs) in NAFLD and normal tissues using the R data package. We investigated protein interactions, correlations, and functional enrichment of these genes. Key genes were identified employing multiple machine learning techniques. Immunoinfiltration analyses were conducted to discern differences in immune cell populations between NAFLD patients and controls. Key gene expression was validated using a cell model. Analysis of GEO datasets, comprising 206 NAFLD samples and 10 controls, revealed two key PRGs (TIRAP, and GSDMD). Combining these genes yielded an area under the curve (AUC) of 0.996 for diagnosing NAFLD. In an external dataset, the AUC for the two key genes was 0.825. Nomogram, decision curve, and calibration curve analyses further validated their diagnostic efficacy. These genes were implicated in multiple pathways associated with NAFLD progression. Immunoinfiltration analysis showed significantly lower numbers of various immune cell types in NAFLD patient samples compared to controls. Single sample gene set enrichment analysis (ssGSEA) was employed to assess the immune microenvironment. Finally, the expression of the two key genes was validated in cell NAFLD model using qRT-PCR. We developed a prognostic model for NAFLD based on two PRGs, demonstrating robust predictive efficacy. Our findings enhance the understanding of pyroptosis in NAFLD and suggest potential avenues for therapeutic exploration.

Although breakthroughs have been achieved in gastric cancer (GC) therapy with immune checkpoint inhibitors (ICIs) targeting programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1), the acquisition of high response rate remains a huge challenge for clinicians. It is imperative to identify novel biomarkers for predicting response to immunotherapy and explore alternative therapeutic strategy for GC.

The transcriptomic profiles and clinical information of GC patients from The Cancer Genome Atlas (TCGA)-stomach adenocarcinoma (STAD) database was used to screen differentially expressed lncRNAs between the tumor specimens and the paracancerous tissues. The TargetScan, miRDB and miRcode database were then utilized to construct competing endogenous RNA (ceRNA) networks and identify pivotal lncRNAs. An independent dataset from GEO (GSE70880) and 23 pairs of GC specimens of our cohort were subsequently performed for external validity. The relationship between clinical variables and gene expression were evaluated by Kruskal-wallis test and Wilcoxon signed-rank. The prognostic value of the candidate genes was assessed using Kaplan-Meier analysis and Cox regression models. CIBERSORT and Gene set enrichment analysis (GSEA) were used to determine immune cell infiltration. Gastric adenocarcinoma AGS cells and human embryonic kidney 293T (HEK293T) cells with knockdown of LINC01094 were generated by siRNA transfection, followed by detecting the alteration of the target miRNA and PD-L1/PD-L2 by RT-qPCR. Besides, the interaction between lncRNA and the miRNA-PD-L1/PD-L2 axis were verified by dual luciferase reporter assay.

Twenty-two intersecting lncRNAs were identified to be PD-L1/PD-L2-related lncRNAs and LINC01094-miR-17-5p-PD-L1/PD-L2 was constructed as a potential ceRNA network. LINC01094 was increased in tumor specimens than adjacent normal samples and was positively associated with advanced tumor stages and EBV and MSI status. Furthermore, LINC01094 expression was an independent risk factor for poor overall survival (OS) in GC patients. CD8+ T cell exhaustion-related genes were enriched in high-LINC01094 tissues and high-PD-L2 group. A strong positive association of LINC01094 expression was established with M2 macrophages, IL-10+ TAM, as well as PD-L1 and PD-L2 levels, therefore a LINC01094-miR-17-5p-IL-10 network was proposed in macrophages. Using the exoRBase database, LINC01094 was assumed in blood exosomes of GC patients The results of knockdown experiments and luciferase reporter assays revealed that LINC01094 interacted with miR-17-5p and served as a miRNA sponge to regulate the expression of PD-L1 and PD-L2.

LINC01094 dually regulates the expression of PD-L1 and PD-L2 and shapes the immunosuppressive tumor microenvironment via sponging miR-17-5p. LINC01094 may serve as a potential prognostic predictor and therapeutic target in GC.

Colorectal cancer (CRC) is one of the most common non-cutaneous malignancies, causing significant mortality and a substantial burden. This study aims to explore the role of KIAA1429 (also known as vir-like m6A methyltransferase associated [VIRMA]) protein in the radioresistance of CRC. CRC cells and a radioresistant cell line were cultured, and KIAA1429 expression was detected. After the down-regulation of KIAA1429, its effect on the radioresistance and ferroptosis of cancer cells was analyzed. The role of ferroptosis in radioresistance was verified. The binding relationship among long non-coding RNA endogenous Bornavirus-like nucleoprotein 3, pseudogene (lncRNA EBLN3P), microRNA (miR)-153-3p, and KIAA1429 was analyzed. KIAA1429 and lncRNA EBLN3P were highly expressed in CRC, while miR-153-3p was poorly expressed. KIAA1429 and lncRNA EBLN3P were further increased/decreased in the radioresistant cells. KIAA1429 knockdown decreased the survival rate of the radioresistant cell line after X-ray irradiation and increased gamma H2A histone family member X (γ-H2AX), ferroptosis, and oxidative stress. A ferroptosis inhibitor alleviated the inhibitory effect of KIAA1429 knockdown on radioresistance. KIAA1429-mediated m6A modification up-regulated lncRNA EBLN3P, and lncRNA EBLN3P increased KIAA1429 by competitively binding to miR-153-3p. miR-153-3p silencing or lncRNA EBLN3P overexpression attenuated the promotion of ferroptosis and the inhibition of radioresistance induced by KIAA1429 knockdown. Overall, KIAA1429-mediated m6A modification up-regulated lncRNA EBLN3P expression, and lncRNA EBLN3P increased KIAA1429 expression by competitively binding to miR-153-3p, thus reducing ferroptosis and increasing the radioresistance of CRC.

The fascinating role of SPRR3 in various malignant tumors has prompted extensive research to unravel its expression patterns and prognostic significance. To comprehensively investigate SPRR3, we leveraged multiple datasets containing invaluable biomedical information, specifically focusing on the comparative analysis of SPRR3 gene expression levels across different cancer types. Meticulous examination of lung adenocarcinoma allowed us to delve deeper into the correlation between SPRR3 expression and its molecular biological functions. Our comprehensive analysis encompassed 33 malignant tumors, and the results unveiled significant differential expression of SPRR3 across a range of malignancies. Moreover, this aberrant expression of SPRR3 was observed to be closely associated with poorer prognosis in these malignant tumors. Notably, our investigation also unearthed a compelling link between SPRR3 and immune infiltrating cells in lung adenocarcinoma. The utilization of receiver operating characteristic (ROC) curves and survival curves in our study illustrated the immense potential of SPRR3 as a highly accurate predictor of cancer. These findings further emphasize the possibility of SPRR3 serving as a promising diagnostic and prognostic biomarker for a diverse array of cancers.

Long noncoding RNAs (lncRNA) have a critical role in colorectal cancer (CRC) development and progression. However, the role of the lncRNA HOXB-AS4 in CRC remains unclear. In this study, we found that HOXB-AS4 was markedly upregulated in tumor tissues compared to precancerous tissues. Loss-of-function assays in HT29 and SW480 cells confirmed that knockdown of HOXB-AS4 inhibited proliferation, migration, and promoted apoptosis. In addition, HOXB-AS4 was shown to regulate histone deacetylase 7 (HDAC7) expression by acting as a molecular sponge to bind to and adsorb miR-140-5p. These findings were confirmed by the dual-luciferase reporter assay. Functional recovery experiments further demonstrated the crucial role of the HOXB-AS4/miR-140-5p/HDAC7 axis in modulating the malignant phenotype of CRC cells. Collectively, our data suggested that HOXB-AS4 regulated the malignant tumor aggression of HT29 and SW480 cells through the miR-140-5p/HDAC7 axis and PI3K/AKT signaling pathway. Our study provides novel insights into the mechanism of action of HOXB-AS4 in CRC and highlights its potential use as a targeted therapy.

Colorectal cancer (CRC) being one of the most common malignancies, has a significant death rate, especially when detected at an advanced stage. In most cases, the fundamental aetiology of CRC remains unclear despite the identification of several environmental and intrinsic risk factors. Numerous investigations, particularly in the last ten years, have indicated the involvement of epigenetic variables in this type of cancer. The development, progression, and metastasis of CRC are influenced by long non-coding RNAs (lncRNAs), which are significant players in the epigenetic pathways. LncRNAs are implicated in diverse pathological processes in CRC, such as liver metastasis, epithelial to mesenchymal transition (EMT), inflammation, and chemo-/radioresistance. It has recently been determined that CRC cells and tissues exhibit dysregulation of tens of oncogenic and tumor suppressor lncRNAs. Serum samples from CRC patients exhibit dysregulated expressions of several of these transcripts, offering a non-invasive method of detecting this kind of cancer. In this review, we outlined the typical paradigms of the deregulated lncRNA which exert significant role in the underlying molecular mechanisms of CRC initiation and progression. We comprehensively discuss the role of lncRNAs as innovative targets for CRC prognosis and treatment.

Alcohol-related liver disease (ALD) is a worldwide burden. Cuproptosis has been shown to play a key role in the development of several diseases. However, the role and mechanisms of cuproptosis in ALD remain unclear.

The RNA-sequencing data of ALD liver samples were downloaded from the Gene Expression Omnibus (GEO) database. Bioinformatical analyses were performed using the R data package. We then identified key genes through multiple machine learning methods. Immunoinfiltration analyses were used to identify different immune cells in ALD patients and controls. The expression levels of key genes were further verified.

We identified three key cuproptosis-related genes (CRGs) (DPYD, SLC31A1, and DBT) through an in-depth analysis of two GEO datasets, including 28 ALD samples and eight control samples. The area under the curve (AUC) value of these three genes combined in determining ALD was 1.0. In the external datasets, the three key genes had AUC values as high as 1.0 and 0.917, respectively. Nomogram, decision curve, and calibration curve analyses also confirmed these genes' ability to predict the diagnosis. These three key genes were found to be involved in multiple pathways associated with ALD progression. We confirmed the mRNA expression of these three key genes in mouse ALD liver samples. Regarding immune cell infiltration, the numbers of B cells, CD8 (+) T cells, NK cells, T-helper cells, and Th1 cells were significantly lower in ALD patient samples than in control liver samples. Single sample gene set enrichment analysis (ssGSEA) was then used to estimate the immune microenvironment of different CRG clusters and CRG-related gene clusters. In addition, we calculated CRG scores through principal component analysis (PCA) and selected Sankey plots to represent the correlation between CRG clusters, gene clusters, and CRG scores. Finally, the three key genes were confirmed in mouse ALD liver samples and liver cells treated with ethanol.

We first established a prognostic model for ALD based on 3 CRGs and robust prediction efficacy was confirmed. Our investigation contributes to a comprehensive understanding of the role of cuproptosis in ALD, presenting promising avenues for the exploration of therapeutic strategies.

Necroptosis is intimately associated with the initiation and progression of colon adenocarcinoma (COAD). However, studies on necroptosis-related genes (NRGs) and the regulating long non-coding RNAs (NRGlncRNAs) in the context of COAD are limited. We retrieved the cancer genome atlas (TCGA) to collect datasets of NRGs and NRGlncRNAs on COAD patients. The risk model constructed using Cox and least absolute shrinkage and selection operator (LASSO) regression was then employed to identify NRGs and NRGlncRNAs with prognostic significance. Subsequently, we validated the results using gene expression omnibus (GEO) datasets from different populations, conducted Mendelian randomization (MR) analysis to explore the potential causal relationships between prognostic NRGs and COAD, and conducted cell experiments to verify the expression of prognostic NRGlncRNAs in COAD. Furthermore, we explored potential pathways and regulatory mechanisms of these prognostic NRGlncRNAs and NRGs in COAD through enrichment analysis, immune cell correlation analysis, tumor microenvironment analysis, immune checkpoint analysis, tumor sample clustering, and so on. We identified eight NRGlncRNAs (AC245100.5, AP001619.1, LINC01614, AC010463.3, AL162595.1, ITGB1-DT, LINC01857, and LINC00513) used for constructing the prognostic model and nine prognostic NRGs (AXL, BACH2, CFLAR, CYLD, IPMK, MAP3K7, ATRX, BRAF, and OTULIN) with regulatory relationships with them, and their validation was performed using GEO and GWAS datasets, as well as cell experiments, which showed largely consistent results. These prognostic NRGlncRNAs and NRGs modulate various biological functions, including immune inflammatory response, oxidative stress, immune escape, telomere regulation, and cytokine response, influencing the development of COAD. Additionally, stratified analysis of the high-risk and low-risk groups based on the prognostic model revealed elevated expression of immune cells, increased expression of tumor microenvironment cells, and upregulation of immune checkpoint gene expression in the high-risk group. Finally, through cluster analysis, we identified tumor subtypes, and the results of cluster analysis were essentially consistent with the analysis between risk groups. The prognostic NGRlncRNAs and NRGs identified in our study serve as prognostic indicators and potential therapeutic targets for COAD, providing a theoretical basis for the clinical diagnosis and treatment of COAD and offering guidance for further research.

LncRNA HAND2-AS1 is a novel cancer regulator, but the role and mechanisms of HAND2-AS1 involved with colon cancer (CC) progression remains unknown. The purpose of this research was to figure out how HAND2-AS1 regulates the progression of CC. Using qRT-PCR, we studied expression levels of miR-3118, HAND2-AS1, and ZG16 in CC tissues and cells. Protein levels of apoptosis-related proteins (Bax and Bcl-2) and ZG16 were quantified by western blotting. In vitro function analysis referred to western blotting, wound healing assay and CCK-8. The binding association among miR-3118, HAND2-AS1, and ZG16 was investigated using luciferase reporter and RIP assays. The functional role of HAND2-AS1 was analyzed using xenograft tumor models in vivo. In tissues and cells of CC, HAND2-AS1 was downregulated. We observed that HAND2-AS1 overexpression declined CC cell proliferation and migration while facilitating apoptosis. We further verified that when HAND2-AS1 is overexpressed it reduced CC tumor development in vivo. In CC cells and tissues, miR-3118 competed with HAND2-AS1 and was elevated. Further it was noted that the HAND2-AS1 when overexpressed, lessened the survival of CC cells, however overexpression of miR-3118 restored these changes. ZG16 was shown to be a target of miR-3118, it was found that ZG16 was downregulated in CC tissue and cells. We observed, high expression of ZG16 partially restored the enhanced malignant phenotype caused by miR-3118 overexpression. HAND2-AS1 inhibited CC progression by upregulating ZG16 expression through sponging miR-3118. Hence, HAND2-AS1/miR-3118/ZG16 axis could be a possible new target for CC treatment.

The dependence of tumor cells on glycolysis provides essential energy and raw materials for their survival and growth. Recent research findings have indicated that long chain non-coding RNAs (LncRNAs) have a key regulatory function in the tumor glycolytic pathway and offer new opportunities for cancer therapy. LncRNAs are analogous to a regulatory key during glycolysis. In this paper, we review the mechanisms of LncRNA in the tumor glycolytic pathway and their potential therapeutic strategies, including current alterations in cancer-related energy metabolism with lncRNA mediating the expression of key enzymes, lactate production and transport, and the mechanism of interaction with transcription factors, miRNAs, and other molecules. Studies targeting LncRNA-regulated tumor glycolytic pathways also offer the possibility of developing new therapeutic strategies. By regulating LncRNA expression, the metabolic pathways of tumor cells can be interfered with to inhibit tumor growth and metastasis, thus affecting the immune and drug resistance mechanisms of tumor cells. In addition, lncRNAs have the capacity to function as molecular markers and target therapies, thereby contributing novel strategies and approaches to the field of personalized cancer therapy and prognosis evaluation. In conclusion, LncRNA, as key molecules regulating the tumor glycolysis pathway, reveals a new mechanism of abnormal metabolism in cancer cells. Future research will more thoroughly investigate the specific mechanisms of LncRNA glycolysis regulation and develop corresponding therapeutic strategies, thereby fostering new optimism for the realization of precision medicine.

Glioma is a primary brain tumor that grows quickly, has an unfavorable prognosis, and can spread intracerebrally. Glioma cells rely on glucose as the major energy source, and glycolysis plays a critical role in tumorigenesis and progression. Substrate utilization shifts throughout glioma progression to facilitate energy generation and biomass accumulation. This metabolic reprogramming promotes glioma cell proliferation and metastasis and ultimately decreases the efficacy of conventional treatments. Non-coding RNAs (ncRNAs) are involved in several glucose metabolism pathways during tumor initiation and progression. These RNAs influence cell viability and glucose metabolism by modulating the expression of key genes of the glycolytic pathway. They can directly or indirectly affect glycolysis in glioma cells by influencing the transcription and post-transcriptional regulation of oncogenes and suppressor genes. In this review, we discussed the role of ncRNAs in the metabolic reprogramming of glioma cells and tumor microenvironments and their abnormal expression in the glucometabolic pathway in glioma. In addition, we consolidated the existing theoretical knowledge to facilitate the use of this emerging class of biomarkers as biological indicators and potential therapeutic targets for glioma.

Multi-organ metastasis has been the main cause of death in patients with Gastric cancer (GC). The prognosis for patients with metastasized GC is still very poor. Long noncoding RNAs (lncRNAs) always been reported to be closely related to cancer metastasis.

In this paper, the aberrantly expressed lncRNA CADM2-AS1 was identified by lncRNA-sequencing in clinical lymph node metastatic GC tissues. Besides, the role of lncRNA CADM2-AS1 in cancer metastasis was detected by Transwell, Wound healing, Western Blot or other assays in vitro and in vivo. Further mechanism study was performed by RNA FISH, Dual-luciferase reporter assay and RT-qPCR. Finally, the relationship among lncRNA CADM2-AS1, miR-5047 and NOTCH4 in patient tissues was detected by RT-qPCR.

In this paper, the aberrantly expressed lncRNA CADM2-AS1 was identified by lncRNA-sequencing in clinical lymph node metastatic GC tissues. Besides, the role of lncRNA CADM2-AS1 in cancer metastasis was detected in vitro and in vivo. The results shown that overexpression of the lncRNA CADM2-AS1 promoted GC metastasis, while knockdown inhibited it. Further mechanism study proved that lncRNA CADM2-AS1 could sponge and silence miR-5047, which targeting mRNA was NOTCH4. Elevated expression of lncRNA CADM2-AS1 facilitate GC metastasis by up-regulating NOTCH4 mRNA level consequently. What's more, the relationship among lncRNA CADM2-AS1, miR-5047 and NOTCH4 was further detected and verified in metastatic GC patient tissues.

LncRNA CADM2-AS1 promoted metastasis in GC by targeting the miR-5047/NOTCH4 signaling axis, which may be a potential target for GC metastasis.

Colon Cancer (CC) incidence has sharply grown in recent years. Long non-coding RNAs (lncRNA) are produced by a group of non-protein-coding genes, and have important functions in controlling gene expression and impacting the biological features of various malignancies including CC.

Our research focused on examining the function of lncRNAs in the development of colon cancer. To this end, we selected and analyzed a dataset (GSE104836) from the GEO database, which contained information about the expression of mRNAs and lncRNAs in both colon cancer tissues and normal adjacent paired tumor tissues. The DESeq2 R package in Bioconductor was used to identify differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) that showed differences in expression levels. Next, by literature review of previous studies, we chose two lncRNAs (FENDRR and LINC00092) for additional studies. To validate our findings, a series of tests were performed on a total of 31 tumor tissues and normal paired adjacent tumor tissues. The lncRNA expression levels were assessed in tumor tissues as well as in surrounding normal tumor tissues.

The data confirmed that just two particular lncRNAs, FENDRR and LINC00092, had considerably decreased expression levels throughout all stages of cancer. In addition, the survival assay was conducted using the GEPIA2 software, revealing that a reduced expression of FENDRR is correlated with a reduced overall survival. Furthermore, our investigation using receiver operating characteristic (ROC) methodology revealed that these two lncRNAs had significant discriminatory ability between colon cancer and normal tissues. To determine the cause of the decrease in the activity of these two long non-coding RNAs (lncRNAs), we used methylation-specific PCR (MSP) to examine the methylation pattern of their promoter regions. Our investigation revealed hypermethylation in the promoter regions of FENDRR and LINC00092 within tumor tissues compared to normal adjacent tumor tissues.

Taken together, our findings revealed the lncRNAs signatures as potential therapeutic targets and molecular diagnostic biomarkers in colon cancer. Furthermore, the evidence provided substantiates the important role of promoter methylation in regulating the expression levels for both of these lncRNAs.

This research aimed to probe the expression of long noncoding RNA TMEM147 antisense RNA 1 (TMEM147-AS1)/micro-RNA (miR)-124/signal transducer and activator of transcription 3 (STAT3) axis in estrogen receptor (ER)-positive breast cancer (BC).

Sixty ER-positive BC patients undergoing surgical treatment were gathered. TMEM147-AS1, miR-124, and STAT3 expression levels in BC cells and tissues were measured. The binding sites of TMEM147-AS1 and miR-124, miR-124, and STAT3 were analyzed and validated. The miR-124, STAT3 overexpression (oe) sequences, TMEM147-AS1 oe, and interference sequences and their control sequences were planned and cells were transfected to assess their functions in BC cells biological functions.

TMEM147-AS1, as well as STAT3 was extremely expressed and miR-124 was lowly expressed in BC cells and tissues. Interference with TMEM147-AS1 restrained ER-positive BC cell malignant activities. Mechanistically, TMEM147-AS1 could competitively bind miR-124 in refraining miR-124 expression, and STAT3 was a target gene of miR-124. Oe of miR-124 effectively reversed the enhancement of BC cell proliferation and invasion induced by TMEM147-AS1 upregulation. Oe of STAT3 could reverse the inhibitory effect of miR-124 on BC cell malignant behaviors.

TMEM147-AS1 has oncogenic activity in ER-positive BC, which may be a result of the altered miR-124/STAT3 axis. Therefore, targeting the TMEM147-AS1/miR-124/STAT3 axis may be a target for ER-positive BC therapy.

Antisense long non-coding RNA (AS-lncRNA) represents a novel class of RNA molecules. In recent years, it has been discovered that AS-lncRNAs play crucial roles in various biological processes, particularly in the onset and progression of tumors. Skull base tumors, originating from the base of the brain, exhibit specific expression patterns of AS-lncRNA which correlate significantly with clinical characteristics. This makes AS-lncRNA a promising candidate as a tumor marker. Functional studies have revealed that AS-lncRNAs can regulate gene expression by acting as miRNA sponges and interacting with RBPs. Consequently, they play pivotal roles in tumor cell cycle, apoptosis, angiogenesis, invasion, and metastasis processes. Further exploration into the mechanisms of AS-lncRNA in tumors holds substantial theoretical significance for deeper insights into the etiology, pathogenesis, and RNA dynamics of skull base tumors. Moreover, AS-lncRNA could serve as molecular markers or potential targets for early diagnosis. Their potential extends to efficacy assessment, prognosis prediction, and gene therapy, suggesting broad clinical applications. In summary, AS-lncRNA emerges as a promising molecular marker implicated in the onset and progression of skull base tumors.

CeRNA axis is an important way to regulate the occurrence and development of Nasopharyngeal carcinoma (NPC). Although the research on inducing cuproptosis of tumor cells is in the early stage of clinical practice, its mechanism of action is still of great significance for tumor treatment, including NPC. However, the regulation mechanism of cuproptosis in NPC by ceRNA network remains unclear.

The ceRNA network related to the survival of nasopharyngeal carcinoma related genes was constructed by bioinformatics. Dual-luciferase reporter assay and other experiments were used to prove the conclusion.

Our findings indicate that the AC008083.2/miR-142-3p axis drives STRN3 to promote the malignant progression of NPC. By performing enrichment analysis and phenotypic assays, we demonstrated that the changes in the expressions of AC008083.2/miR-142-3p/NPC can affect the proliferation of NPC. Mechanistically, luciferase reporter gene assays suggested that AC008083.2 acts as a ceRNA of miR-142-3p to regulate the content of STRN3. Furthermore, the regulations of STRN3 and the malignant progression of NPC by AC008083.2 depends on miR-142-3p to some extent.

Our study reveals an innovative ceRNA regulatory network in NPC, which can be considered a new potential target for diagnosing and treating NPC.

Ameloblastoma (AB) is a common odontogenic tumor that develops in the mouth. Despite its benign nature, AB exhibits significant invasiveness leading to tumor metastasis and high postoperative recurrence rates. Studies have shown a relationship between the occurrence and development of various tumors and non-coding RNA (ncRNA). NcRNA, transcribed from the genomes of mammals and other complex organisms, are often products of alternative splicing and processing into smaller products. MicroRNA (miRNA), circular RNA (circRNA), and long non-coding RNA (lncRNA) are the main types of ncRNA. NcRNA play increasingly significant roles in the pathogenesis of human cancers, regulating their occurrence and progression as oncogenes or tumor suppressors. They are involved in tumor development and progression through alternative splicing of pre-mRNA, transcriptional regulation, mRNA stability, protein translation, and chromatin remodeling and modification. The importance of ncRNA in AB has received significant attention in recent years. However, the biological functions and mechanisms of ncRNA in AB remain largely unknown. In this review, we not only explore the functions and roles of ncRNA in AB, but also describe and envision their potential functional roles as biomarkers in AB diagnosis. In particular, we highlight the potential of miR-29a as a molecular marker for diagnosis and therapy. As promising novel therapeutic targets, the biological functions of ncRNA need further study, which is indispensable.

The role of long noncoding RNA (lncRNA) in tumors, particularly in gastrointestinal tumors, has gained significant attention. Accumulating evidence underscores the interaction between various lncRNAs and diverse molecular pathways involved in cancer progression. One such pivotal pathway is the PI3K/AKT pathway, which serves as a crucial intracellular mechanism maintaining the balance among various cellular physiological processes for normal cell growth and survival. Frequent dysregulation of the PI3K/AKT pathway in cancer, along with aberrant activation, plays a critical role in driving tumorigenesis. LncRNAs modulate the PI3K/AKT signaling pathway through diverse mechanisms, primarily by acting as competing endogenous RNA to regulate miRNA expression and associated genes. This interaction significantly influences fundamental biological behaviors such as cell proliferation, metastasis, and drug resistance. Abnormal expression of numerous lncRNAs in gastrointestinal tumors often correlates with clinical outcomes and pathological features in patients with cancer. Additionally, these lncRNAs influence the sensitivity of tumor cells to chemotherapy in multiple types of gastrointestinal tumors through the abnormal activation of the PI3K/AKT pathway. These findings provide valuable insights into the mechanisms underlying gastrointestinal tumors and potential therapeutic targets. However, gastrointestinal tumors remain a significant global health concern, with increasing incidence and mortality rates of gastrointestinal tumors over recent decades. This review provides a comprehensive summary of the latest research on the interactions of lncRNA and the PI3K/AKT pathway in gastrointestinal tumor development. Additionally, it focuses on the functions of lncRNAs and the PI3K/AKT pathway in carcinogenesis, exploring expression profiles, clinicopathological characteristics, interaction mechanisms with the PI3K/AKT pathway, and potential clinical applications.