Long non-coding RNAs (lncRNAs) have been evidenced to function as pivotal modulators in tumorigenesis. LncRNA SNHG25 is highly expressed in colorectal cancer (CRC), but its specific function in CRC has not been elucidated yet. The expression of SNHG25, miR-329-3p, and PPP2R2D was determined using qRT-PCR analysis and western blot analysis. The influence of the SNHG25/miR-329-3p/PPP2R2D axis on CRC progression was explored through in vitro assays including CCK-8, colony formation, wound healing, Transwell assays and in vivo orthotopic xenografts assay. The interaction between miR-329-3p and SNHG25 or PPP2R2D was examined by RNA pull-down, RIP, and luciferase reporter assays. SNHG25 presented high expression in CRC cell lines. Silencing of SNHG25 suppressed the malignant phenotypes of CRC cells in vitro and tumor growth in vivo. MiR-329-3p, which displayed low expression in CRC cells, was sponged by SNHG25. Downregulation of miR-329-3p reversed the inhibitory effects of SNHG25 silencing on CRC cell malignant behaviors. Additionally, PPP2R2D served as a miR-329-3p downstream target, whose expression was downregulated by overexpressing miR-329-3p. Importantly, overexpression of PPP2R2D rescued SNHG25 silencing-induced repression on CRC cell malignancy. SNHG25 plays a carcinogenic role in CRC via regulation of the miR-329-3p/PPP2R2D axis.

The online version contains supplementary material available at 10.1007/s10616-025-00753-3.

Prostate cancer (PCa) is a leading cause of cancer-related morbidity and mortality in men worldwide. Despite advancements in diagnosis and treatment, challenges such as late-stage detection, therapeutic resistance, and the complexity of castration-resistant prostate cancer (CRPC) persist. Long non-coding RNAs (LncRNAs) play critical roles in PCa progression through epigenetic regulation, transcriptional and post-transcriptional modulation, and immune response regulation. This review highlights the molecular mechanisms by which LncRNAs influence PCa development, treatment resistance, and immune regulation, emphasizing their potential as biomarkers and therapeutic targets. We also discuss future research directions to advance precision medicine in PCa.

Pancreatic cancer (PC) is a common gastrointestinal cancer with high invasiveness and high mortality. Curcumin is a natural polyphenol with anti-tumor activity against different cancers, including PC. Curcumin has been verified to mediate the expression of circular RNAs (circRNAs) to inhibit tumor development. This study aimed to explore the function and regulatory mechanism of curcumin on circ_0079440 in PC. PC cells were treated with different concentrations of curcumin (0, 5, 10 or 15 μM) for 24 h. Gene expression in PC cells and tissues was detected using RT-qPCR. Cell malignant phenotypes were determined by functional assays. The levels of EMT-related proteins were tested using western blot. RNA interaction was determined using RNA pulldown assay, luciferase reporter assay and RIP assay. The results showed that curcumin suppressed cell proliferative, migratory, and invasive capabilities, and weakened epithelial-mesenchymal transition (EMT) in a concentration-dependent way. Circ_0079440 was expressed at a high level in PC and its level was reduced via curcumin administration in PC cells. Rescue assays showed that circ_0079440 overexpression reversed the suppressive effects of curcumin on PC cell malignant phenotypes. Furthermore, in the xenograft mouse models, curcumin treatment inhibited tumor growth and metastasis, and circ_0079440 upregulation reversed the function of curcumin. Additionally, circ_0079440 was revealed to bind to miR-522-3p to upregulate eukaryotic initiation factor 4A1 (EIF4A1) expression in PC cells. EIF4A1 expression was also downregulated by curcumin, and EIF4A1 overexpression abolished the suppressive functions of curcumin. Moreover, EIF4A overexpression or miR-522-3p inhibition counteracted the anti-tumor effects of circ_0079440 depletion on PC development. To sum up, curcumin suppresses PC development by targeting the circ_0079440/miR-522-3p/EIF4A1 pathway, which might provide novel therapeutic targets for treatment of PC.

Lung cancer has a higher incidence and mortality rate than other cancers, especially non-small cell lung cancer (NSCLC), accounting for 85% of the cases. The role of the circDENND4C/miR-200b/matrix metalloproteinase-9 (MMP-9) regulatory axis in NSCLC remains largely unknown.

NSCLC cell lines were used to examine the expression of circDENND4C, miR-200b, and MMP-9 via qRT-PCR or Western blot. The target relationship of circDENND4C, miR-200b, and MMP-9 was examined by RNA fluorescence in situ hybridization (RNA-FISH), immunofluorescence (IF), dual-luciferase reporter system, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. Then, a cell count kit-8 (CCK-8) experiment, flow cytometry, and migration/invasion assays were performed to assess the biological function of circDENND4C, miR-200b, and MMP-9 by transfecting with their overexpression or knockout plasmids in A549 cells. Finally, the proteins related to cell adhesion and tight junction were further tested by Western blot and IF.

circDENND4C and MMP-9 were found to be highly expressed in NSCLC cell lines, while miR-200b was lowly expressed in NSCLC cell lines. Moreover, circDENND4C could sponge miR-200b to target MMP-9. Subsequently, it was observed that knockdown of circDENND4C and MMP-9 or the upregulation of miR-200b repressed cell proliferation and cell cycle progression, increased cell apoptosis, and hindered cell migration and invasion. Finally, it was also found that the circDENND4C/miR-200b/MMP-9 regulatory axis might be involved with cell adhesion and tight junction to influence tumor metastasis.

Altogether, our study reveals a novel regulatory loop in which the circDENND4C/miR-200b/MMP-9 axis may modulate NSCLC progression, indicating potential biomarkers for the diagnosis or treatment of NSCLC.

Neurofibromatosis (NF) is identified as genetic disorder characterized by multiple tumors on nerve tissues. NF1 is the most prevalent form, identified by neurofibromas and skin changes. NF1 is the most prevalent neurofibromatosis disorder, distinct from the rarer NF2 and schwannomatosis (SWN) conditions. NF2, including NF2-related SWN (NF2-SWN), predominantly involves schwannoma formation and differs from NF1 in its genetic basis and clinical presentation. Despite the established genetic basis of NF, effective treatments remain scarce. Long non-coding RNAs (lncRNAs) have emerged as important regulators of gene expression, impacting pathways vital to tumor biology. This review explores the lncRNAs role in NF pathogenesis along with their potential as therapeutic targets. LncRNAs such as ANRIL and H19 show dysregulated expression in NF, influencing signaling pathways like Ras/MAPK and JAK/STAT, thereby contributing to tumor development. Understanding these interactions sheds light on the molecular mechanisms underlying NF and highlights lncRNAs as potential biomarkers of diagnosis and prognosis of NF. Additionally, therapeutic strategies targeting lncRNAs with antisense oligonucleotides (ASOs) or CRISPR-Cas9 offer promising treatment options. The present review emphasizes crucial role of lncRNAs in NF pathogenesis and their promise to create innovative treatments, aiming to improve patient outcomes and meet the urgent need for effective NF therapies.

The non-coding RNAs (ncRNAs) comprise a large part of human genome that mainly do not code for proteins. Although ncRNAs were first believed to be non-functional, the more investigations highlighted tthe possibility of ncRNAs in controlling vital biological processes. The length of long non-coding RNAs (lncRNAs) exceeds 200 nucleotidesand can be present in nucleus and cytoplasm. LncRNAs do not translate to proteins and they have been implicated in the regulation of tumorigenesis. On the other hand, One way cells die is by a process called autophagy, which breaks down proteins and other components in the cytoplasm., while the aberrant activation of autophagy allegedly involved in the pathogenesis of diseases. The autophagy exerts anti-cancer activity in pre-cancerous lesions, while it has oncogenic function in advanced stages of cancers. The current overview focuses on the connection between lncRNAs and autophagy in urological cancers is discussed. Notably, one possible role for lncRNAs is as diagnostic and prognostic variablesin urological cancers. The proliferation, metastasis, apoptosis and therapy response in prostate, bladder and renal cancers are regulated by lncRNAs. The changes in autophagy levels can also influence the apoptosis, proliferation and therapy response in urological tumors. Since lncRNAs have modulatory functions, they can affect autophagy mechanism to determine progression of urological cancers.

Human bone marrow mesenchymal stem cells (hBMSCs) are adult stem cells residing in the bone marrow, characterized by their capacity for multi-directional differentiation, self-renewal, migration, and engraftment. Serving as seed cells, BMSCs play a pivotal role in the regeneration of bone defects. Hence, investigating the transcription factors and signaling pathways involved in the regulation of osteogenic differentiation in BMSCs holds significant importance. Recent research has unveiled that certain circular RNAs (circRNAs) can function as molecular sponges, influencing the osteogenic differentiation process of mesenchymal stem cells. However, many circRNAs remain undiscovered, and their precise mechanisms remain elusive. Therefore, the objective of this study is to construct an osteogenic differentiation-related circRNA-miRNA-mRNA network in hBMSCs. Subsequently, through bioinformatics analysis, we constructed a ceRNA network related to the osteogenic differentiation ability of hBMSCs, comprising 22 circRNAs, 17 miRNAs, and 15 mRNAs. The potential circRNA-miRNA-mRNA axes, including the role of hsa_circ_0001600 in promoting the osteogenic differentiation of hBMSCs through the targeted regulation of hsa-miR-542-3p, were validated through in vitro experiments.

Long non-coding RNAs (lncRNAs) have been identified as important participants in several biological functions, particularly their complex interactions with the KRAS pathway, which provide insights into the significant roles lncRNAs play in cancer development. The KRAS pathway, a central signaling cascade crucial for cell proliferation, survival, and differentiation, stands out as a key therapeutic target due to its aberrant activation in many human cancers. Recent investigations have unveiled a myriad of lncRNAs, such as H19, ANRIL, and MEG3, intricately modulating the KRAS pathway, influencing both its activation and repression through various mechanisms, including epigenetic modifications, transcriptional regulation, and post-transcriptional control. These lncRNAs function as fine-tuners, delicately orchestrating the balance required for normal cellular function. Their dysregulation has been linked to the development and progression of multiple malignancies, including lung, pancreatic, and colorectal carcinomas, which frequently harbor KRAS mutations. This scrutiny delves into the functional diversity of specific lncRNAs within the KRAS pathway, elucidating their molecular mechanisms and downstream effects on cancer phenotypes. Additionally, it underscores the diagnostic and prognostic potential of these lncRNAs as indicators for cancer detection and assessment. The complex regulatory network that lncRNAs construct within the context of the KRAS pathway offers important insights for the creation of focused therapeutic approaches, opening new possibilities for precision medicine in oncology. However, challenges such as the dual roles of lncRNAs in different cancer types and the difficulty in therapeutically targeting these molecules highlight the ongoing debates and need for further research. As ongoing studies unveil the complexities of lncRNA-mediated KRAS pathway modulation, the potential for innovative cancer interventions becomes increasingly promising.

Hepatocellular carcinoma (HCC) poses a significant threat due to its highly aggressive and high recurrence characteristics, necessitating urgent advances in diagnostic and therapeutic approaches. Long non-coding RNAs exert vital roles in HCC tumorigenesis, however the mechanisms of their expression regulation and functions are not fully elucidated yet. Herein, we identify that a novel tumor suppressor 'lnc-PIK3R1' was significantly downregulated in HCC tissues, which was correlated with poor prognosis. Functionally, lnc-PIK3R1 played tumor suppressor roles to inhibit the proliferation and mobility of HCC cells, and to impede the distant implantation of xenograft in mice. Mechanistic studies revealed that lnc-PIK3R1 interacted with miR-1286 and alleviated the repression on GSK3B by miR-1286. Notably, pharmacological inhibition of GSK3β compromised the tumor suppression effect by lnc-PIK3R1, confirming their functional relevance. Moreover, we identified that oncogenic YY1 acts as a specific transcriptional repressor to downregulate the expression of lnc-PIK3R1 in HCC. In summary, this study highlights the tumor-suppressive effect of lnc-PIK3R1, and provides new insights into the regulation of GSK3β expression in HCC, which would benefit the development of innovative intervention strategies for HCC.

High Mobility Group A2 (HMGA2) oncofetal proteins are a distinct category of Transcription Factors (TFs) known as "architectural factors" due to their lack of direct transcriptional activity. Instead, they modulate the three-dimensional structure of chromatin by binding to AT-rich regions in the minor grooves of DNA through their AT-hooks. This binding allows HMGA2 to interact with other proteins and different regions of DNA, thereby regulating the expression of numerous genes involved in carcinogenesis. Consequently, multiple mechanisms exist to finely control HMGA2 protein expression at various transcriptional levels, ensuring precise concentration adjustments to maintain cellular homeostasis. During embryonic development, HMGA2 protein is highly expressed but becomes absent in adult tissues. However, recent studies have revealed its re-elevation in various cancer types. Extensive research has demonstrated the involvement of HMGA2 protein in carcinogenesis at multiple levels. It intervenes in crucial processes such as cell cycle regulation, apoptosis, angiogenesis, epithelial-to-mesenchymal transition, cancer cell stemness, and DNA damage repair mechanisms, ultimately promoting cancer cell survival. This comprehensive review provides insights into the HMGA2 protein, spanning from the genetic regulation to functional protein behavior. It highlights the significant mechanisms governing HMGA2 gene expression and elucidates the molecular roles of HMGA2 in the carcinogenesis process.

Co-infection with porcine reproductive and respiratory syndrome virus (PRRSV) and Haemophilus parasuis (HPS) has severely restricted the healthy development of pig breeding. Exploring disease resistance of non-coding RNAs in pigs co-infected with PRRSV and HPS is therefore critical to complement and elucidate the molecular mechanisms of disease resistance in Kele piglets and to innovate the use of local pig germplasm resources in China. RNA-seq of lungs from Kele piglets with single-infection of PRRSV or HPS and co-infection of both pathogens was performed. Two hundred and twenty-five differentially expressed long non-coding RNAs (DElncRNAs) and 30 DEmicroRNAs (DEmiRNAs) were identified and characterized in the PRRSV and HPS co-infection (PRRSV-HPS) group. Compared with the single-infection groups, 146 unique DElncRNAs, 17 unique DEmiRNAs, and 206 target differentially expressed genes (DEGs) were identified in the PRRSV-HPS group. The expression patterns of 20 DEmiRNAs and DElncRNAs confirmed by real-time quantitative polymerase chain reaction (RT-qPCR) were consistent with those determined by high-throughput sequencing. In the PRRSV-HPS group, the target DEGs were enriched in eight immune Gene Ontology terms relating to two unique DEmiRNAs and 16 DElncRNAs, and the unique target DEGs participated the host immune response to pathogens infection by affecting 15 immune-related Kyoto Encyclopedia of Genes and Genomes enrichment pathways. Notably, competitive endogenous RNA (ceRNA) networks of different groups were constructed, and the ssc-miR-671-5p miRNA was validated as a potential regulatory factor to regulate DTX4 and AEBP1 genes to achieve innate antiviral effects and inhibit pulmonary fibrosis by dual-luciferase reporter assays. These results provided insight into further study on the molecular mechanisms of resistance to PRRSV and HPS co-infection in Kele piglets.

Long non-coding RNAs are an essential component of competing endogenous RNA regulatory axes and play their role by sponging microRNAs and interfering with the regulation of gene expression. Because of the broadness of competing endogenous RNA interaction networks, they may help investigate treatment targets in complicated disorders.

This study performed a systematic scoping review to assess verified loops of competing endogenous RNAs in retinoblastoma, emphasizing the competing endogenous RNAs axis related to long non-coding RNAs. We used a six-stage approach framework and the PRISMA guidelines. A systematic search of seven databases was done to locate suitable papers published before February 2022. Two reviewers worked independently to screen articles and collect data.

Out of 363 records, fifty-one articles met the inclusion criteria, and sixty-three axes were identified in desired articles. The majority of the research reported several long non-coding RNAs that were experimentally verified to act as competing endogenous RNAs in retinoblastoma: XIST/NEAT1/MALAT1/SNHG16/KCNQ1OT1, respectively. At the same time, around half of the studies investigated unique long non-coding RNAs.

Understanding the many features of this regulatory system may aid in elucidating the unknown etiology of Retinoblastoma and providing novel molecular targets for therapeutic and clinical applications.

Polycystic ovary syndrome (PCOS) is the most common condition affecting women of reproductive age globally. PCOS continues to be the largest contributing factor to female infertility despite significant progress in our knowledge of the molecular underpinnings and treatment of the condition. The fact that PCOS is a very diverse condition makes it one of the key reasons why we haven't been able to overcome it. Non-coding RNAs (ncRNAs) are implicated in the development of PCOS, according to growing evidence. However, it is unclear how the complex regulatory relationships between the many ncRNA types contribute to the growth of this malignancy. Competing endogenous RNA (ceRNA), a recently identified mechanism in the RNA world, suggests regulatory interactions between various RNAs, including long non-coding RNAs (lncRNAs), microRNAs (miRNAs), transcribed pseudogenes, and circular RNAs (circRNAs). Recent studies on PCOS have shown that dysregulation of multiple ceRNA networks (ceRNETs) between these ncRNAs plays crucial roles in developing the defining characteristics of PCOS development. And it is believed that such a finding may open a new door for a deeper comprehension of PCOS's unexplored facets. In addition, it may be able to provide fresh biomarkers and effective therapy targets for PCOS. This review will go over the body of information that exists about the primary roles of ceRNETs before highlighting the developing involvement of several newly found ceRNETs in a number of PCOS characteristics.

Despite substantial evidence emphasizing the pleiotropic benefits of exercise for the prevention and treatment of various diseases, the underlying biological mechanisms have not been fully elucidated. Several exercise benefits have been attributed to signaling molecules that are released in response to exercise by different tissues such as skeletal muscle, cardiac muscle, adipose, and liver tissue. These signaling molecules, which are collectively termed exerkines, form a heterogenous group of bioactive substances, mediating inter-organ crosstalk as well as structural and functional tissue adaption. Numerous scientific endeavors have focused on identifying and characterizing new biological mediators with such properties. Additionally, some investigations have focused on the molecular targets of exerkines and the cellular signaling cascades that trigger adaption processes. A detailed understanding of the tissue-specific downstream effects of exerkines is crucial to harness the health-related benefits mediated by exercise and improve targeted exercise programs in health and disease. Herein, we review the current in vivo evidence on exerkine-induced signal transduction across multiple target tissues and highlight the preventive and therapeutic value of exerkine signaling in various diseases. By emphasizing different aspects of exerkine research, we provide a comprehensive overview of (i) the molecular underpinnings of exerkine secretion, (ii) the receptor-dependent and receptor-independent signaling cascades mediating tissue adaption, and (iii) the clinical implications of these mechanisms in disease prevention and treatment.

Hepatocellular carcinoma (HCC) continues to endanger human health worldwide. Regulatory networks of competing endogenous RNAs (ceRNAs) play important roles in HCC. TP53 is the second most often altered gene in HCC and has a significant role in regulating target genes such as miRNAs and lncRNAs.

Data from patients with TP53 mutation were collected through the cBioPortal database and differential analysis was performed to screen RNAs related to TP53 mutation. The lncRNA-miRNA-mRNA relationship was predicted by the miRcode, miRDB, and TargetScan databases. The ceRNA networks were screened and visualized by Cytoscape. Core ceRNA networks were generated by differential analysis, coexpression analysis, prognostic analysis and subcellular localization. Finally, methylation, mutation, PPI, GSEA, immunity and drug sensitivity analyses of MEX3A were performed to determine the role of MEX3A in HCC.

We identified 1508 DEmRNAs, 85 DEmiRNAs and 931 DElncRNAs and obtained a ceRNA network including 28 lncRNAs, 4 miRNAs and 31 mRNAs. Twenty hub DERNAs in the TP53-altered-related ceRNA network were screened out by Cytoscape and the core ceRNA network (LINC00491/TCL6-hsa-miR-139-5p-MEX3A) was obtained by multiple analyses. In addition, we discovered that the methylation level of MEX3A was decreased and the mutation frequency was raised in HCC. Furthermore, elevated MEX3A expression was associated with alterations in the HCC immunological microenvironment.

We successfully constructed a reciprocal ceRNA network, which could provide new ideas for exploring HCC mechanisms and therapeutic approaches.

During the secretory phase of the menstrual cycle, endometrial fibroblast cells begin to change into large epithelial-like cells called decidual cells in a process called decidualization. This differentiation continues more broadly in the endometrium and forms the decidual tissue during early pregnancy. The cells undergoing decidualization as well as the resulting decidual cells, support successful implantation and placentation during early pregnancy. This study was carried out to identify new potentially important long non-coding RNA (lncRNA) genes that may play a role in human endometrial stromal fibroblast cells (hESF) undergoing decidualization in vitro, and several were found. The expression of nine was further characterized. One of these, AC027288.3, showed a dramatic increase in the expression of hESF cells undergoing decidualization. When AC027288.3 expression was targeted, the ability of the cells to undergo decidualization as determined by the expression of decidualization marker protein-coding genes was significantly altered. The most affected markers of decidualization whose expression was significantly reduced were FOXO1, FZD4, and INHBA. Therefore, AC027288.3 may be a major upstream regulator of the WNT-FOXO1 pathway and activin-SMAD3 pathways previously shown as critical for hESF decidualization. Finally, we explored possible regulators of AC027288.3 expression during human ESF decidualization. Expression was regulated by cAMP and progesterone. Our results suggest that AC027288.3 plays a role in hESF decidualization and identifies several other lncRNA genes that may also play a role.

Perineural invasion (PNI) is an essential form of tumor metastasis in multiple malignant cancers, such as pancreatic cancer, prostate cancer, and head and neck cancer. Growing evidence has revealed that pancreatic cancer recurrence and neuropathic pain positively correlate with PNI. Therefore, targeting PNI is a proper strategy for pancreatic cancer treatment. Exosomal lncRNA derived from pancreatic cancer cells is an essential component of the tumor microenvironment. However, whether exosomal lncXIST derived from pancreatic cancer cells can promote PNI and its exact mechanism remains to be elucidated. We show that lncXIST mediates nerve-tumor crosstalk via exosomal delivery. Our data reveal that exosomal lncXIST derived from pancreatic cancer cells is delivered to neural cells and promotes their release of glial-cell-line-derived neurotrophic factor (GDNF), essential in facilitating the PNI of pancreatic cancer. Mechanistically, microRNA-211-5p negatively regulates GDNF, and lncXIST serves as a miR-211-5p sponge. The function of exosomes in the dynamic interplay between nerves and cancer is confirmed in both in vivo and in vitro PNI models. Therefore, targeting pancreatic cancer cell-derived exosomal lncXIST may provide clues for a promising approach for developing a new strategy to combat PNI of pancreatic cancer.

Genetic assessment of tumors following neoadjuvant immunotherapy helps identifying targets that mediate anti-tumor immunity. In this study, we explored dysregulated RNAs in esophageal squamous cell carcinoma samples after neoadjuvant immunotherapy using deep sequencing and high-throughput screening. We identified 584 differentially expressed messenger RNAs (mRNAs), 67 differentially expressed microRNAs (miRNAs), and 1,047 differentially expressed long non-coding RNAs (lncRNAs) using differential expression analysis. Competing endogenous RNAs closely related to esophageal squamous cell carcinoma were selected via a combined Pearson's correlation test and weighted correlation network analysis. After validation using survival analysis and dry-lab and wet-lab-based studies, we identified the I-miR-378-5p-APOC1/CEP55 as a critical pathway for esophageal squamous cell carcinoma progression after neoadjuvant immunotherapy. Tumor immune infiltration analysis showed that APOC1 and CEP55 expression is associated with immune regulatory pathways and the function of multiple infiltrating immune cells. We investigated the mechanism of esophageal squamous carcinoma progression after neoadjuvant immunotherapy from the perspective of the mRNA-miRNA-lncRNA network. Furthermore, we identified accurate novel therapeutic targets and prognostic biomarkers, introduced novel perspectives to immunotherapy studies, and laid the foundation for the clinical treatment of patients with esophageal squamous carcinoma.

Rotavirus (RV) is the primary etiological agent of virus-associated gastroenteritis in infants, causing 200,000 childhood death annually. Despite the availability of vaccines, rotaviral diarrhea continues to be a severe issue in underdeveloped nations in Asia and Africa. The situation demands continual studies on host-rotavirus interactions to understand disease pathogenesis and develop effective antiviral therapeutics. Long non-coding RNAs (lncRNAs), which are a subset of non-coding RNAs of more than 200 nucleotides in length, are reported to play a regulatory function in numerous viral infections. Virus infection often alters the host transcriptome including lncRNA that are differentially expressed either to play an antiviral role or to be advantageous towards virus propagation. In the current study, qPCR array-based expression profiling of host lncRNAs was performed in rotavirus-infected HT-29 cells that identified the lncRNA SLC7A11-AS1 to be upregulated during RV infection. Knockdown of SLC7A11-AS1 conspicuously reduced RV titers implying its pro-viral significance. RV-induced SLC7A11-AS1 downregulates the gene SLC7A11/xCT that encodes the light chain subunit of the system XC- cystine-glutamate exchange transporter, leading to decrease in intracellular glutathione level and increase in lipid peroxidation, which are signature features of ferroptotic pathway. Ectopic expression of xCT also abrogated RV infection by reversing the virus optimized levels of intracellular GSH and lipid ROS levels. Cumulatively, the study reveals that RV infection triggers ferroptotic cell death via SLC7A11-AS1/xCT axis to facilitate its own propagation.

There is no doubt that the incidence of cancer sufferers is rising in the world, and it is estimated that in the next several decades, the number of people suffering from malignancies or the cancer rate will double. Diagnostic and therapeutic targeting of noncoding RNAs (ncRNAs), especially microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), represent an excellent approach for cancer diagnosis and treatment, as well as many other diseases. One of the latest miRNAs is miR-4492, upregulating some genes in tumor tissues including ROMO1, HLA-G, NKIRAS2, FOXK1, and UBE2C. It represents an attractant example of a miRNA acting at multiple levels to affect the same malignancy hallmark. Based on the studies, miR-4492 plays a key role in several cancers such as, breast cancer, bladder cancer, osteosarcoma, glioblastoma multiforme, hepatocellular carcinoma, colorectal cancer, and ovarian cancer. Putting it all together, identifying the precise mechanisms of miR-4492 in the pathogenesis of cancer, could pave the way to find better diagnostic and therapeutic strategies for cancer sufferers. For this reason, it might be a novel potential diagnostic biomarker and therapeutic target for neoplasms.

Cancer is a complicated illness that spreads indefinitely owing to epigenetic, genetic, and genomic alterations. Cancer cell multidrug susceptibility represents a severe barrier in cancer therapy. As a result, creating effective therapies requires a better knowledge of the mechanisms driving cancer development, progress, and resistance to medications. The human genome is predominantly made up of long non coding RNAs (lncRNAs), which are currently identified as critical moderators in a variety of biological functions. Recent research has found that changes in lncRNAs are closely related to cancer biology. The vascular endothelial growth factor (VEGF) signalling system is necessary for angiogenesis and vascular growth and has been related to an array of health illnesses, such as cancer. LncRNAs have been identified to alter a variety of cancer-related processes, notably the division of cells, movement, angiogenesis, and treatment sensitivity. Furthermore, lncRNAs may modulate immune suppression and are being investigated as possible indicators for early identification of cancer. Various lncRNAs have been associated with cancer development and advancement, serving as cancer-causing or suppressing genes. Several lncRNAs have been demonstrated through research to impact the VEGF cascade, resulting in changes in angiogenesis and tumor severity. For example, the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been shown to foster the formation of oral squamous cell carcinoma and the epithelial-mesenchymal transition by stimulating the VEGF-A and Notch systems. Plasmacytoma variant translocation 1 (PVT1) promotes angiogenesis in non-small-cell lung cancer by affecting miR-29c and boosting the VEGF cascade. Furthermore, lncRNAs regulate VEGF production and angiogenesis by interacting with multiple downstream signalling networks, including Wnt, p53, and AKT systems. Identifying how lncRNAs engage with the VEGF cascade in cancer gives beneficial insights into tumor biology and possible treatment strategies. Exploring the complicated interaction between lncRNAs and the VEGF pathway certainly paves avenues for novel ways to detect better accurately, prognosis, and cure cancers. Future studies in this area could open avenues toward the creation of innovative cancer therapy regimens that enhance the lives of patients.

To explore the regulatory networks that underlie the development of chemoresistance in bladder cancer.

We analyzed profiles of differentially expressed long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), microRNAs (miRNAs) and messenger RNA (mRNAs) in gemcitabine-resistant/sensitive bladder cancer cells using next-generation sequencing data.

Hundreds of differentially expressed lncRNAs and miRNAs and thousands of circRNAs and mRNAs were identified. Bioinformatics analysis revealed the chromosomal localizations, classification and coexpression of mRNAs, as well as candidates for cis and trans regulation by lncRNAs. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of differentially expressed mRNAs and circRNAs indicated important functional roles of coregulated RNAs, thus establishing competing endogenous RNA (ceRNA) and protein-protein interactions networks that may underlie chemoresistance in bladder cancer. We demonstrated that lncRNA LINP1 can act as a ceRNA by inhibiting miR-193a-5p to increase TP73 expression; and that lncRNA ESRG and hsa_circ_0075881 can simultaneously bind miR-324-3p to increase ST6GAL1 expression. Modulation of ceRNA network components using ablation and overexpression approaches contributed to gemcitabine resistance in bladder cancer cells.

These results elucidate mechanisms by which lncRNAs and circRNAs coregulate the development of bladder cancer cell resistance to gemcitabine, thus laying the foundation for future research to identify biomarkers and disease targets.

Porcine epidemic diarrhea virus (PEDV) causes porcine epidemic diarrhea (PED), a highly infectious disease, which has resulted in huge economic losses for the pig industry. To date, the pathogenic and immune response mechanism was not particularly clear. The purpose of this study was to investigate the pathogenic and immune responses of pigs infected with PEDV.In this study, 12 Min pigs were randomly selected without taking colostrum. At 3 days old, eight piglets were infected with 1 mL of PEDV solution (10 TCID50/ml), and the remaining four piglets were handled by 1 mL of 0.9% normal saline. Within the age of 7 days old, four piglets died and were considered as the death group. Correspondingly, four alive individuals were classified into the resistance group. Tissues of the duodenum, jejunum, ileum, colon, cecum, and rectum of piglets in the three groups were collected to measure the PEDV content. Additionally, the jejunum was used for the measurements and analyses of Hematoxylin-eosinstaining (HE), immunohistochemical sections, and transcriptomics. The phenotypes of Min piglets infected with PEDV showed that the viral copy numbers and jejunal damage had significant differences between the death and resistance groups. We also observed the transcriptome of the jejunum, and the differentially expressed (DE) analysis observed 6,585 DE protein-coding genes (PCGs), 3,188 DE long non-coding RNAs (lncRNAs), and 350 DE microRNAs (miRNAs), which were mainly involved in immune response and metabolic pathways. Furthermore, the specific expressed molecules for each group were identified, and 97 PCGs,108 lncRNAs, and 51 miRNAs were included in the ceRNA-regulated networks. By weighted gene co-expression network analysis (WGCNA) and transcription factor (TF) prediction, 27 significant modules and 32 significant motifs (E-value < 0.05) annotated with 519 TFs were detected. Of these TFs, 53 were DE PCGs. In summary, the promising key PCGs, lncRNAs, and miRNAs related to the pathogenic and immunological response of pigs infected with PEDV were detected and provided new insights into the pathogenesis of PEDV.

A sight-threatening, cataract is a common degenerative disease of the ocular lens. This study aimed to explore the regulatory mechanism of age-related cataract (ARC) formation and progression.

Cataracts in Sprague Dawley rats were induced by adopting the method that injected selenite subcutaneously in the nape. We performed high-throughput RNA sequencing technology to identify the mRNA and microRNA(miRNA) expression profiles of the capsular membrane of the lens from Na2SeO3-induced and saline-injected Sprague Dawley rats. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were carried out to forecast the regulatory and functional role of mRNAs in cataracts by DAVID and Metascape. The protein-protein interaction(PPI) network of differentially expressed mRNA(DEmRNAs) was built via the STRING. Target miRNAs of hub genes were predicted by miRBD and TargetScan. Furthermore, differentially expressed miRNA(DEmiRNAs) were selected as hub genes' targets, validated by quantitative real-time polymerase chain reaction(qRT-PCR), and a DEmiRNA-DEmRNA regulatory network was constructed via Cytoscape.

In total, 329 DEmRNAs including 40 upregulated and 289 downregulated genes were identified. Forty seven DEmiRNAs including 29 upregulated and 18 downregulated miRNAs were detected. The DEmRNAs are involved in lens development, visual perception, and aging-related biological processes. A protein-protein interaction network including 274 node genes was constructed to explore the interactions of DEmRNAs. Furthermore, a DEmiRNA-DEmRNA regulatory network related to cataracts was constructed, including 8 hub DEmRNAs, and 8 key DEmiRNAs which were confirmed by qRT-PCR analysis.

We identified several differentially expressed genes and established a miRNA-mRNA-regulated network in a Na2SeO3-induced Sprague Dawley rat cataract model. These results may provide novel insights into the clinical treatment of cataracts, and the hub DEmRNAs and key DEmiRNAs could be potential therapeutic targets for ARC.

Biomarkers are biomolecules used to identify or predict the presence of a specific disease or condition. They play an important role in early diagnosis and may be crucial for treatment. MicroRNAs (miRNAs), a group of small non-coding RNAs, are more and more regarded as promising biomarkers for several reasons. Dysregulation of miRNAs has been linked with development of several diseases, including many different types of cancer, and abnormal levels can be present in early stages of tumor development. Because miRNAs are stable molecules secreted and freely circulating in blood and urine, they can be sampled with little or no invasion. Here, we present an overview of the current literature, focusing on the types of cancers for which dysregulation of miR-665 has been associated with disease progression, recurrence, and/or prognosis. It needs to be emphasized that the role of miR-665 sometimes seems ambiguous, in the sense that it can be upregulated in one cancer type and downregulated in another and can even change during the progression of the same cancer. Caution is thus needed before using miR-665 as a biomarker, and extrapolation between different cancer types is not advisable. Moreover, more detailed understanding of the different roles of miR-665 will help in determining its potential as a diagnostic and prognostic biomarker.

Long non-coding RNAs (lncRNAs) play an essential part in controlling gene expression and a variety of biological processes such as immune defense and stress-response. However, whether and how lncRNAs regulate responses of Apis cerana larvae to Ascosphaera apis invasion has remained unclear until now. Here, the identification and structural analysis of lncRNAs in the guts of A. cerana worker larvae were conducted, and the expression profile of larval lncRNAs during the A. apis infection process was then analyzed, followed by an investigation of the regulatory roles of differentially expressed lncRNAs (DElncRNAs) in the host response. In total, 76 sense lncRNAs, 836 antisense lncRNAs, 184 intron lncRNAs, 362 bidirectional lncRNAs, and 2181 intron lncRNAs were discovered in the larval guts. Additionally, 30 known and 9 novel lncRNAs were potential precursors for 36 and 11 miRNAs, respectively. In the three comparison groups, 386, 351, and 272 DElncRNAs were respectively identified, indicating the change in the overall expression pattern of host lncRNAs following the A. apis invasion. Analysis of cis-acting effect showed that DElncRNAs in the 4-, 5-, and 6-day-old comparison groups putatively regulated 55, 30, and 20 up- and down-stream genes, respectively, which were involved in a series of crucial functional terms and pathways, such as MAPK signaling pathway, and cell process. Analysis showed that 31, 8, and 11 DElncRNAs as potential antisense lncRNAs may interact with 26, 8, and 9 sense-strand mRNAs. Moreover, investigation of the competing endogenous RNA (ceRNA) network indicated that 148, 283, and 257 DElncRNAs were putatively regulated. The expression of target genes by targeting corresponding DEmiRNAs included those associated with antioxidant enzymes and immune responses. These results suggested that DElncRNAs played a potential part in the larval guts responding to the A. apis infection through a cis-acting manner and ceRNA mechanisms. Our findings deepen our understanding of interactions between A. cerana larvae and A. apis and offer a basis for clarifying the DElncRNA-mediated mechanisms underlying the host response to fungal invasion.

Epigenetics is a rapidly developing science that has gained a lot of interest in recent years due to the correlation between characteristic epigenetic marks and cardiovascular diseases (CVDs). Epigenetic modifications contribute to a change in gene expression while maintaining the DNA sequence. The analysis of these modifications provides a thorough insight into the cardiovascular system from its development to its further functioning. Epigenetics is strongly influenced by environmental factors, including known cardiovascular risk factors such as smoking, obesity, and low physical activity. Similarly, conditions affecting the local microenvironment of cells, such as chronic inflammation, worsen the prognosis in cardiovascular diseases and additionally induce further epigenetic modifications leading to the consolidation of unfavorable cardiovascular changes. A deeper understanding of epigenetics may provide an answer to the continuing strong clinical impact of cardiovascular diseases by improving diagnostic capabilities, personalized medical approaches and the development of targeted therapeutic interventions. The aim of the study was to present selected epigenetic pathways, their significance in cardiovascular diseases, and their potential as a therapeutic target in specific medical conditions.

Benign prostate hyperplasia (BPH) is the most commonly seen disease among aging males. Transforming growth factor(TGF)-β-mediated epithelial-mesenchymal transition (EMT) and epithelial overproliferation might be central events in BPH etiology and pathophysiology. In the present study, long noncoding RNA MIR663AHG, miR-765, and FOXK1 formed a competing endogenous RNAs network, modulating TGF-β-mediated EMT and epithelial overproliferation in BPH-1 cells. miR-765 expression was downregulated in TGF-β-stimulated BPH-1 cells; miR-765 overexpression ameliorated TGF-β-mediated EMT and epithelial overproliferation in BPH-1 cells. MIR663AHG directly targeted miR-765 and negatively regulated miR-765; MIR663AHG knockdown also attenuated TGF-β-induced EMT and epithelial overproliferation in BPH-1 cells, whereas miR-765 inhibition attenuated MIR663AHG knockdown effects on TGF-β-stimulated BPH-1 cells. miR-765 directly targeted FOXK1 and negatively regulated FOXK1. FOXK1 knockdown attenuated TGF-β-induced EMT and epithelial overproliferation and promoted autophagy in BPH-1 cells, and partially attenuated miR-765 inhibition effects on TGF-β-stimulated BPH-1 cells. In conclusion, this study provides a MIR663AHG/miR-765/FOXK1 axis modulating TGF-β-induced epithelial proliferation and EMT, which might exert an underlying effect on BPH development and act as therapeutic targets for BPH treatment regimens.

Osteoporosis (OP) is characterized by a decrease in osteoblasts and an increase in adipocytes in the bone marrow compartment, alongside abnormal bone/fat differentiation, which ultimately results in imbalanced bone homeostasis. Bone marrow mesenchymal stem cells (BMSCs) can differentiate into osteoblasts and adipocytes to maintain bone homeostasis. Several studies have shown that lncRNAs are competitive endogenous RNAs that form a lncRNA-miRNA network by targeting miRNA for the regulation of bone/fat differentiation in BMSCs; this mechanism is closely related to the corresponding treatment of OP and is important in the development of novel OP-targeted therapies. However, by reviewing the current literature, it became clear that there are limited summaries discussing the effects of the lncRNA-miRNA network on osteogenic/adipogenic differentiation in BMSCs. Therefore, this article provides a review of the current literature to explore the impact of the lncRNA-miRNA network on the osteogenic/adipogenic differentiation of BMSCs, with the aim of providing a new theoretical basis for the treatment of OP.

miRNAs and lncRNAs play a central role in cancer-associated gene regulations. The dysregulated expression of lncRNAs has been reported as a hallmark of cancer progression, acting as an independent prediction marker for an individual cancer patient. The interplay of miRNA and lncRNA decides the variation of tumorigenesis that could be mediated by acting as sponges for endogenous RNAs, regulating miRNA decay, mediating intra-chromosomal interactions, and modulating epigenetic components. This paper focuses on the influence of crosstalk between lncRNA and miRNA on cancer hallmarks such as epithelial-mesenchymal transition, hijacking cell death, metastasis, and invasion. Other cellular roles of crosstalks, such as neovascularization, vascular mimicry, and angiogenesis were also discussed. Additionally, we reviewed crosstalk mechanism with specific host immune responses and targeting interplay (between lncRNA and miRNA) in cancer diagnosis and management.

In the entire world, prostate cancer (PCa) is one of the most common and deadly cancers. Treatment failure is still common among patients, despite PCa diagnosis and treatment improvements. Inadequate early diagnostic markers and the emergence of resistance to conventional therapeutic approaches, particularly androgen-deprivation therapy, are the causes of this. Long non-coding RNAs (lncRNAs), as an essential group of regulatory molecules, have been reported to be dysregulated through prostate tumorigenesis and hold great promise as diagnostic targets. Besides, lncRNAs regulate the malignant features of PCa cells, such as proliferation, invasion, metastasis, and drug resistance. These multifunctional RNA molecules interact with other molecular effectors like miRNAs and transcription factors to modulate various signaling pathways, including AR signaling. This study aimed to compile new knowledge regarding the role of lncRNA through prostate tumorigenesis in terms of their effects on the various malignant characteristics of PCa cells; in light of these characteristics and the significant potential of lncRNAs as diagnostic and therapeutic targets for PCa. AVAILABILITY OF DATA AND MATERIALS: Not applicable.

Wheat sharp eyespot caused by Rhizoctonia cerealis is primarily a severe threat to worldwide wheat production. Currently, there are no resistant wheat cultivars, and the use of fungicides is the primary method for controlling this disease. Elucidating the mechanisms of R. cerealis pathogenicity can accelerate the pace of the control of this disease. Long intergenic noncoding RNAs (lincRNAs) that function in plant-pathogen interactions might provide a new perspective. We systematically analyzed lincRNAs and identified a total of 1,319 lincRNAs in R. cerealis. We found that lincRNAs are involved in various biological processes, as shown by differential expression analysis and weighted correlation network analysis (WGCNA). Next, one of nine hub lincRNAs in the blue module that was related to infection and growth processes, MSTRG.4380.1, was verified to reduce R. cerealis virulence on wheat by a host-induced gene silencing (HIGS) assay. Following that, RNA sequencing (RNA-Seq) analysis revealed that the significantly downregulated genes in the MSTRG.4380.1 knockdown lines were associated mainly with infection-related processes, including hydrolase, transmembrane transporter, and energy metabolism activities. Additionally, 23 novel microRNAs (miRNAs) were discovered during small RNA (sRNA) sequencing (sRNA-Seq) analysis of MSTRG.4380.1 knockdown, and target prediction of miRNAs suggested that MSTRG.4380.1 does not act as a competitive endogenous RNA (ceRNA). This study performed the first genome-wide identification of R. cerealis lincRNAs and miRNAs. It confirmed the involvement of a lincRNA in the infection process, providing new insights into the mechanism of R. cerealis infection and offering a new approach for protecting wheat from R. cerealis. IMPORTANCE Rhizoctonia cerealis, the primary causal agent of wheat sharp eyespot, has caused significant losses in worldwide wheat production. Since no resistant wheat cultivars exist, chemical control is the primary method. However, this approach is environmentally unfriendly and costly. RNA interference (RNAi)-mediated pathogenicity gene silencing has been proven to reduce the growth of Rhizoctonia and provides a new perspective for disease control. Recent studies have shown that lincRNAs are involved in various biological processes across species, such as biotic and abiotic stresses. Therefore, verifying the function of lincRNAs in R. cerealis is beneficial for understanding the infection mechanism. In this study, we reveal that lincRNAs could contribute to the virulence of R. cerealis, which provides new insights into controlling this pathogen.

Pulmonary hypertension (PH) is characterized by a progressive increase in pulmonary arterial pressure and pulmonary vascular resistance. In a short time, it leads to right ventricular failure and, consequently, to death. The most common causes of PH include left heart disease and lung disease. Despite the significant development of medicine and related sciences observed in recent years, we still suffer from a lack of effective treatment that would significantly influence the prognosis and prolong life expectancy of patients with PH. One type of PH is pulmonary arterial hypertension (PAH). The pathophysiology of PAH is based on increased cell proliferation and resistance to apoptosis in the small pulmonary arteries, leading to pulmonary vascular remodeling. However, studies conducted in recent years have shown that epigenetic changes may also lie behind the pathogenesis of PAH. Epigenetics is the study of changes in gene expression that are not related to changes in the sequence of nucleotides in DNA. In addition to DNA methylation or histone modification, epigenetic research focuses on non-coding RNAs, which include microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Preliminary research results give hope that targeting epigenetic regulators may lead to new, potential therapeutic possibilities in the treatment of PAH.

Alternative splicing (AS) is a common and conserved process in eukaryotic gene regulation. It occurs in approximately 95% of multi-exon genes, greatly enriching the complexity and diversity of mRNAs and proteins. Recent studies have found that in addition to coding RNAs, non-coding RNAs (ncRNAs) are also inextricably linked with AS. Multiple different types of ncRNAs are generated by AS of precursor long non-coding (pre-lncRNAs) or precursor messenger RNAs (pre-mRNAs). Furthermore, ncRNAs, as a novel class of regulators, can participate in AS regulation by interacting with the cis-acting elements or trans-acting factors. Several studies have implicated abnormal expression of ncRNAs and ncRNA-related AS events in the initiation, progression, and therapy resistance in various types of cancers. Therefore, owing to their roles in mediating drug resistance, ncRNAs, AS-related factors and AS-related novel antigens may serve as promising therapeutic targets in cancer treatment. In this review, we summarize the interaction between ncRNAs and AS processes, emphasizing their great influences on cancer, especially on chemoresistance, and highlighting their potential values in clinical treatment.

The antler is the unique mammalian organ found to be able to regenerate completely and periodically after loss, and the continuous proliferation and differentiation of mesenchymal cells and chondrocytes together complete the regeneration of the antler. Circular non-coding RNAs (circRNAs) are considered to be important non-coding RNAs that regulate body development and growth. However, there are no reports on circRNAs regulating the antler regeneration process. In this study, full-transcriptome high-throughput sequencing was performed on sika deer antler interstitial and cartilage tissues, and the sequencing results were verified and analyzed. The competing endogenous RNA (ceRNA) network related to antler growth and regeneration was further constructed, and the differentially expressed circRNA2829 was screened out from the network to study its effect on chondrocyte proliferation and differentiation. The results indicated that circRNA2829 promoted cell proliferation and increased the level of intracellular ALP. The analysis of RT-qPCR and Western blot demonstrated that the mRNA and protein expression levels of genes involved in differentiation rose. These data revealed that circRNAs play a crucial regulatory role in deer antler regeneration and development. CircRNA2829 might regulate the antler regeneration process through miR-4286-R+1/FOXO4.

The young shoots of the tea plant Baiye No. 1 display an albino phenotype in the early spring under low environmental temperatures, and the leaves re-green like those of common tea cultivars during the warm season. Periodic albinism is precisely regulated by a complex gene network that leads to metabolic differences and enhances the nutritional value of tea leaves. Here, we identified messenger RNAs (mRNAs), long noncoding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs) to construct competing endogenous RNA (ceRNA) regulatory networks. We performed whole-transcriptome sequencing of 12 samples from four periods (Bud, leaves not expanded; Alb, albino leaves; Med, re-greening leaves; and Gre, green leaves) and identified a total of 6325 differentially expressed mRNAs (DEmRNAs), 667 differentially expressed miRNAs (DEmiRNAs), 1702 differentially expressed lncRNAs (DElncRNAs), and 122 differentially expressed circRNAs (DEcircRNAs). Furthermore, we constructed ceRNA networks on the basis of co-differential expression analyses which comprised 112, 35, 38, and 15 DEmRNAs, DEmiRNAs, DElncRNAs, and DEcircRNAs, respectively. Based on the regulatory networks, we identified important genes and their interactions with lncRNAs, circRNAs, and miRNAs during periodic albinism, including the ceRNA regulatory network centered on miR5021x, the GAMYB-miR159-lncRNA regulatory network, and the NAC035-miR319x-circRNA regulatory network. These regulatory networks might be involved in the response to cold stress, photosynthesis, chlorophyll synthesis, amino acid synthesis, and flavonoid accumulation. Our findings provide novel insights into ceRNA regulatory mechanisms involved in Baiye No. 1 during periodic albinism and will aid future studies of the molecular mechanisms underlying albinism mutants.

Nowadays, there is an increasing concern regarding traumatic brain injury (TBI) worldwide since substantial morbidity is observed after it, and the long-term consequences that are not yet fully recognized. A number of cellular pathways related to the secondary injury in brain have been identified, including free radical production (owing to mitochondrial dysfunction), excitotoxicity (regulated by excitatory neurotransmitters), apoptosis, and neuroinflammatory responses (as a result of activation of the immune system and central nervous system). In this context, non-coding RNAs (ncRNAs) maintain a fundamental contribution to post-transcriptional regulation. It has been shown that mammalian brains express high levels of ncRNAs that are involved in several brain physiological processes. Furthermore, altered levels of ncRNA expression have been found in those with traumatic as well non-traumatic brain injuries. The current review highlights the primary molecular mechanisms participated in TBI that describes the latest and novel results about changes and role of ncRNAs in TBI in both clinical and experimental research.

Long noncoding RNA (lncRNA) is noncoding RNA and have played a key role or be treated as a biomarker in a variety of diseases such as tumors. However, extensive lncRNA analysis for uveitis has not been explored completely. In this study, we analyzed the lncRNAs with altered expression in peripheral blood comprehensively for three major autoimmune diseases (ankylosing spondylitis [AS], Behҫet's disease [BD], and sarcoidosis) to search potential hub gene and molecular mechanism for noninfectious uveitis.

In total, we included 18 patients with AS and 12 patients with sarcoidosis versus 25 controls for GSE18781; we also included 15 patients with BD versus 14 controls for GSE17114 in this study. The lncRNA and messenger RNA (mRNA) expression levels were determined by microarray using serum samples from patients and healthy controls.

Twenty-one lncRNAs and 1073 mRNAs were detected in patients with AS, 4 lncRNAs and 62 mRNAs in patients with BD, and 196 lncRNAs and 5376 mRNAs in patients with sarcoidosis. Thus, we suspected lncRNA XIST and MIAT, mRNA FCGBP, CD247, CTSW, AES, NCR3, TIGIT, CASP5, DUSP2, and TBX21 may be the most possible hub genes for AS, BD, and sarcoidosis. These RNAs were involved in the mitogen-activated protein kinase signaling pathway and inflammatory cytokine pathways.

In this study, comprehensive bioinformatics analysis identified lncRNAs with altered expression in three major autoimmune diseases that may combine with noninfectious uveitis. This study provides novel insights into the molecular pathogenetic mechanisms and key information toward developing new diagnostic biomarkers and special therapeutic targets for noninfectious uveitis in AS, BD, and sarcoidosis.

LncRNAs and their potential mechanisms provide new strategies for prevention and treatment for noninfectious uveitis in patients with AS, BD, and sarcoidosis.

The malignant bone tumor osteosarcoma (OS) was one of the most aggressive tumors. Despite breakthroughs in treatment options for OS recently, the survival rate of patients with metastasis or reoccurring disease has remained unchanged over the last 25 years, at around 20%. lncRNA expression dysregulation is linked to carcinogenesis, advancement, and metastasis. Additionally, the fundamental mechanism of lncRNAs in regulating OS cell biological activity and progression is still being investigated. The expression of miR-873-5p and MALAT1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in OS. The relationship between the expression level of MALAT1 and the survival rate of OS individuals was evaluated by the Kaplan-Meier plotter. The tumor cell's capability of proliferation was determined using the CCK-8. Transwell was used to test the migratory and invasive properties of tumor cells. ROCK1 protein expression was analyzed by western blot, while qRT-PCR was used to detect ROCK1 mRNA expression. Targeted genes of MALAT1 or miR-873-5p were predicted by StarBase2.0. The target association among miR-873-5p and MALAT1 or ROCK1 was confirmed using the luciferase assay. The relationship between ROCK1 and MALAT1 or miR-873-5p expression in OS was investigated using Spearman's correlation analysis. MALAT1 was up-regulated and was linked to a lower survival rate of patients in OS. The malignant behaviors of cells were inhibited by down-regulated MALAT1 in vitro. Dual-luciferase gene experiments confirmed the presence of MALAT1/miR-873-5p/ROCK1 axis. The up-regulated miR-873-5p blocked the promoted effects of MALAT1 on cell behaviors. Over-expressed MALAT1 promoted the malignant behaviors of cells by miR-873-5p/ROCK1 axis in OS.

Benign prostatic hyperplasia (BPH) is a common disease among aging males. We obtained BPH transcriptional signatures by high-throughput RNA sequencing analysis. Accordingly, we determined the differentially expressed RNAs (DERNAs) between BPH tissues and normal prostate tissues. WebGestalt and R package (clusterprofiler) was used to enrichment analysis. Clinical correlations were analyzed using Spearman's coefficient. TargetScan, ENCORI, miRNet, and miRDB databases were used to predict targets' relationships in ceRNA networks. Immunofluorescence staining and qRT-PCR analyses were performed to validate the findings. Microarray analysis of the datasets showed 369 DElncRNAs, 122 DEpseudogenes, 6 DEmiRNAs and 1358 DEmRNAs. DEmRNAs were particularly enriched in the autophagy-related pathways. Following the screening of DEmRNAs and autophagy-related genes (ARGs), 50 DEARGs were selected. MCODE analysis on Cytoscape was performed for the 50 DEARGs, and 3 hub genes (ATF4, XBP1, and PPP1R15A) were obtained. Spearman's correlation analysis showed that the mRNA expression of XBP1 correlated positively with age, total score, and storage score, but negatively with the maximum flow rate. Subsequently, the pseudogene/lncRNA- hsa-miR-222-3p-XBP1 pathway was identified. Our findings elucidate that the pseudogene/lncRNA-hsa-miR-222-3p-XBP1 pathway may play a regulatory role in the occurrence of BPH through autophagy.