• Cancer
• Hallmarks
• LncRNA
• Long Non-coding RNA
• MIAT
• Oncogenic
• Solid malignancies

• Epigenetics
• Naringenin
• Naringin
• circRNA
• lncRNA
• miRNA

• Flavanones/pharmacology
• Epigenesis, Genetic/drug effects
• Humans
• Animals
• MicroRNAs/metabolism
• Antioxidants/pharmacology
• Anti-Inflammatory Agents/pharmacology

• DNA methylation
• Hi-C
• breast cancer
• enhancer
• lncRNA
• promoter

• Humans
• RNA, Long Noncoding/genetics
• Breast Neoplasms/genetics
• Breast Neoplasms/pathology
• DNA Methylation
• Promoter Regions, Genetic
• Female
• Enhancer Elements, Genetic
• CpG Islands/genetics
• Chromatin/genetics
• Chromatin/metabolism
• Gene Expression Regulation, Neoplastic
• Prognosis
• Biomarkers, Tumor/genetics

• 62361047 National Natural Science Foundation of China
• 32160216 National Natural Science Foundation of China

• biomarkers
• ceRNAs
• ceRNETs
• ceRNome
• circRNAs
• lncRNAs
• mTNBC
• metastasis
• microRNAs
• therapeutic targets
• triple-negative breast cancer (TNBC)

• Cancer
• Clinical application
• Non-coding RNA
• Therapeutic targets

• Cancer heterogeneity
• Chromatin remodeling
• DNA methylation
• Drug resistance
• Epigenetic modifications
• Epigenetic therapies
• Gene expression regulation
• Histone modifications

• Cancer
• Metastasis
• MicroRNA
• MicroRNA-155

• Breast cancer
• FOXO3a
• MIAT
• bioinformatics
• ceRNA network
• miRNA29a-3p
• noninvasive bioindicator

• Tarbiat Modares University Tehran, Iran

• Exosomes
• Immune-related hearing loss
• Whole transcriptome sequencing
• lncRNA
• mRNA
• miRNA

• BC
• CeRNET
• CircRNA
• LncRNA
• MiRNA
• NcRNAs

Myocardial infarction–associated transcript (MIAT) is a long noncoding RNA that plays a critical role in a variety of diseases. Accordingly, this study probed into the possible interaction mechanism between MIAT and miR-378a-5p in breast cancer. Concretely, MIAT and miR-378a-5p expressions in breast cancer tissues and cells were measured. After transfection with siMIAT and miR-378a-5p inhibitor, the viability and proliferation of breast cancer cells were examined by cell counting kit-8 and colony formation assays. The expressions of apoptosis-related proteins were detected. According to the results, MIAT was highly expressed in breast cancer tissues and cells. MIAT silencing could decrease Bcl-2 expression, viability, and proliferation of breast cancer cells and increase the expressions of cleaved caspase-3 and Bax. MIAT and miR-378a-5p could directly bind to each other, and MIAT silencing promoted the expression of miR-378a-5p. miR-378a-5p expression was low in breast cancer tissues. The miR-378a-5p inhibitor enhanced the viability and proliferation of breast cancer cells and partially reversed the effects of MIAT silencing on the breast cancer cells. In conclusion, MIAT silencing inhibits the viability and proliferation of breast cancer cells by promoting miR-378a-5p, indicating the potential of MIAT as a new target for the treatment of breast cancer.

• breast cancer
• miat
• mir-378a-5p
• viability
• proliferation

• K-mer profiles
• RNA binding sites
• lncRNA functional similarity

• breast cancer biomarkers
• estrogen receptor alpha
• estrogen signaling
• lncRNAs

• Animals
• Dual Specificity Phosphatase 1/metabolism
• Dual-Specificity Phosphatases/genetics
• Dual-Specificity Phosphatases/metabolism
• Mesoderm/metabolism
• Mice
• Mitogen-Activated Protein Kinases/metabolism
• Mouse Embryonic Stem Cells/metabolism
• Phosphoserine
• Phosphothreonine
• Phosphotyrosine

• Grantová Agentura České Republiky
• Masarykova Univerzita

• Implant
• Osseointegration
• Titanium
• miR-155-5p
• microRNAs

• ERK pathway
• IGFBP7-AS1
• Odontogenetic differentiation
• SHED
• miR-155-5p
• miR-335-3p

• atherosclerosis
• cancer
• cardiomyopathy
• inflammation
• non-coding RNAs
• oxidative stress

• Breast carcinoma
• CDC25A
• MiR-100-5p
• Migration and invasion
• Proliferation

Myocardial infarction associated transcript (MIAT) is identified as a long chain non-coding RNA (lncRNA), which was associated with myocardial infarction susceptibility. While intense efforts have been made to elucidate the relationship between MIAT and carcinogenesis, the tumor immunoreaction of MIAT remains elusive. Thus, this study aimed to investigate the role of MIAT in the immunoregulation of breast cancer (BC) and further explore the better clinical significance.

The differential expression of MIAT between BC and normal/adjacent tissues was compared using Wilcoxon rank sum test. The diagnostic and prognostic values of elevated MIAT expression in BC tissues were unveiled via receiver operating characteristic (ROC) analysis and KM-plotter analysis. Limma and edgeR package were used to identify differentially expressed genes (DEGs) and microRNAs (DEMs) from TCGA database respectively. A co-expression dataset was constructed to comprehensively understand the relationship between MIAT and DEGs based on the Pearson correlation coefficient. Furthermore, GO and KEGG analyses were conducted to predict the potential functions of MIAT. We next intersected immune-related genes (IRGs) from ImmPort database with MIAT-co-expressed genes to obtain MIAT-co-expressed IRGs, in order to construct MIAT-microRNA (miRNA)-mRNA network. And the correlation between MIAT and tumor-infiltrating immune cells (TICs) and immunophenoscore (IPS) analysis was analyzed by TIMER and CIBERSORT. Finally, the reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression profiles of MIAT in serum samples.

The expression levels of MIAT were notably higher in BC than in normal or adjacent tissues. And MIAT expression could be used as a prognostic indicator of mortality risk in patients with BC in different aspects. Moreover, the enrichment analyses suggested that MIAT was strongly involved in BC immune response. In addition, TIMER database and CIBERSORT analyses indicated that MIAT was significantly correlated with 13 types of TICs (B cells, dendritic cells, neutrophils, CD8 T cells, CD4 memory resting T cells, CD4 memory activated T cells, gamma delta T cells, M1 macrophages, plasma cells, activated NK cells, monocytes, M2 macrophages, activated mast cells). Simultaneously, the IPS analysis implied that the higher the MIAT expression, the better the immunotherapy effect. The ROC curve analysis showed that the area under the curve (AUC) value of MIAT was 0.86 (sensitivity = 87.80%, specificity = 75.61%). And the high MIAT expression in serum was positive related to TNM stage (P = 0.032) and lymph node metastasis (P = 0.028).

MIAT may be a valuable noninvasive diagnostic biomarker for BC and is associated with tumor-infiltrating immune cells in tumor microenvironment, suggesting MIAT as a potential target for future treatment of BC.

• BC
• biomarker
• immune cells
• immune regulation
• lncRNA MIAT
• tumor-infiltrating

Osteosarcoma, derived from primitive mesenchymal cells, is the most common primary solid malignant tumor of bone. The cause of osteosarcoma remains unclear. In recent years, the role of non-coding sequences in regulating protein expression in tumors has been paid more and more attention, especially long non-coding RNA (lncRNA). We speculate that SRY-box transcription factor 21 antisense divergent transcript 1 (SOX21-AS1) can regulate the expression of the mechanistic target of rapamycin kinase (mTOR) and Kruppel-like factor 4 (KLF4) through sponging hsa-mir-7-5p and hsa-mir-145-5p. We knocked lncRNA SOX21-AS1 into the genome of 143B cells through CRISPR/Cas9, then screened out a monoclonal cell line. Detect the transcription level and protein expression level of the above-mentioned related genes, and cell proliferation. Then, ginsenoside Rg3 was added to culture the cell line knocked into lncRNA SOX21-AS1, and the expression levels of lncRNA SOX21-AS1, hsa-mir-7-5p, hsa-mir-145-5p, mTOR, and KLF4 were detected by RT-qPCR and Western blot. Cell proliferation method detects cell viability, explores the molecular mechanism of lncRNA SOX21-AS1 in osteosarcoma, and checks whether it can be used as a potential drug target for the treatment of osteosarcoma. Our results demonstrate that the overexpression of lncRNA SOX21-AS1 up-regulates mTOR and KLF4 by sponging hsa-mir-7-5p and hsa-mir-145-5p, and ultimately regulates the proliferation of osteosarcoma. It is proved that ginsenoside Rg3 can inhibit the cell proliferation of osteosarcoma by reducing the expression level of lncRNA SOX21-AS1. It provides an alternative for the treatment of osteosarcoma in the future.

• KLF4
• Osteosarcoma
• hsa-mir-145-5p
• hsa-mir-7-5p
• lncRNA SOX21-AS1
• mTOR

Mitogen-activated protein kinases (MAPKs) are essential for proper cell functioning as they regulate many molecular effectors. Careful regulation of MAPKs is therefore required to avoid MAPK pathway dysfunctions and pathologies. The mammalian genome encodes about 200 phosphatases, many of which dephosphorylate the MAPKs and bring them back to an inactive state. In this review, we focus on the normal and pathological functions of dual-specificity phosphatase 9 (DUSP9)/MAP kinase phosphatases-4 (MKP-4). This cytoplasmic phosphatase, which belongs to the threonine/tyrosine dual-specific phosphatase family and was first described in 1997, is known to dephosphorylate ERK1/2, p38, JNK and ASK1, and thereby to control various MAPK pathway cascades. As a consequence, DUSP9 plays a major role in human pathologies and more specifically in cardiac dysfunction, liver metabolic syndromes, diabetes, obesity and cancer including drug response and cell stemness. Here, we recapitulate the mechanism of action of DUSP9 in the cell, its levels of regulation and its roles in the most frequent human diseases, and discuss its potential as a therapeutic target.

• MAP kinase phosphatase
• cancer
• dual-specificity phosphatase
• metabolic syndromes
• mitogen-activated protein kinase
• sex differences
• therapy

• Animals
• Dual-Specificity Phosphatases/chemistry
• Dual-Specificity Phosphatases/genetics
• Dual-Specificity Phosphatases/metabolism
• Female
• Gene Expression Regulation, Enzymologic
• Heart Diseases/enzymology
• Humans
• MAP Kinase Signaling System
• Male
• Metabolic Diseases/enzymology
• Metabolic Networks and Pathways
• Mice
• Mitogen-Activated Protein Kinase Phosphatases/chemistry
• Mitogen-Activated Protein Kinase Phosphatases/genetics
• Mitogen-Activated Protein Kinase Phosphatases/metabolism
• Models, Molecular
• Mouse Embryonic Stem Cells/enzymology
• Neoplasms/enzymology
• Protein Conformation
• Sex Characteristics
• Tissue Distribution

• Biomarker; Long non-coding RNA (lncRNA); MicroRNA; Regulation mechanism; Triple-negative breast cancer (TNBC)

• Female
• Gene Expression Regulation, Neoplastic
• Humans
• MicroRNAs/analysis
• MicroRNAs/physiology
• Neoadjuvant Therapy
• RNA, Long Noncoding/analysis
• RNA, Long Noncoding/physiology
• Triple Negative Breast Neoplasms/drug therapy
• Triple Negative Breast Neoplasms/etiology
• Triple Negative Breast Neoplasms/genetics
• Triple Negative Breast Neoplasms/pathology

Abnormal long non-coding RNAs (lncRNAs) expression has been documented to have oncogene or tumor suppressor functions in the development and progression of cancer, emerging as promising independent biomarkers for molecular cancer stratification and patients’ prognosis. Examining the relationship between lncRNAs and the survival rates in malignancies creates new scenarios for precision medicine and targeted therapy. Breast cancer (BRCA) is a heterogeneous malignancy. Despite advances in its molecular classification, there are still gaps to explain in its multifaceted presentations and a substantial lack of biomarkers that can better predict patients’ prognosis in response to different therapeutic strategies. Here, we performed a re-analysis of gene expression data generated using cDNA microarrays in a previous study of our group, aiming to identify differentially expressed lncRNAs (DELncRNAs) with a potential predictive value for response to treatment with taxanes in breast cancer patients. Results revealed 157 DELncRNAs (90 up- and 67 down-regulated). We validated these new biomarkers as having prognostic and predictive value for breast cancer using in silico analysis in public databases. Data from TCGA showed that compared to normal tissue, MIAT was up-regulated, while KCNQ1OT1, LOC100270804, and FLJ10038 were down-regulated in breast tumor tissues. KCNQ1OT1, LOC100270804, and FLJ10038 median levels were found to be significantly higher in the luminal subtype. The ROC plotter platform results showed that reduced expression of these three DElncRNAs was associated with breast cancer patients who did not respond to taxane treatment. Kaplan–Meier survival analysis revealed that a lower expression of the selected lncRNAs was significantly associated with worse relapse-free survival (RFS) in breast cancer patients. Further validation of the expression of these DELncRNAs might be helpful to better tailor breast cancer prognosis and treatment.

• biomarkers
• breast cancer
• docetaxel
• lncRNAs
• prognosis

• Antineoplastic Agents/therapeutic use
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Breast Neoplasms/drug therapy
• Breast Neoplasms/genetics
• Breast Neoplasms/pathology
• Docetaxel/therapeutic use
• Drug Resistance, Neoplasm
• Female
• Humans
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Survival Analysis
• Transcriptome

• PP7080
• UHRF1BP1
• lung adenocarcinoma
• miR-670-3p

Tuberculosis (TB) remains a major public health problem. Long non-coding RNAs (lncRNAs) are important regulators of gene expression. In this study, we explored the association between the expression of lncRNA AC007128.1 and TB susceptibility.

Three single-nucleotide polymorphisms (SNPs) (rs12333784, rs6463794, and rs720964) of lncRNA AC007128.1 were selected using the 1000 Genomes Project database and offline software Haploview V4.2, and were genotyped by a customized 2×48-Plex SNPscan™ Kit.

We identified two differentially expressed lncRNA including AC007128.1 and AP001065.3 in comparisons of expression profiles between ATB vs. LTBI, LTBI vs. HCs, and AC700128.1 expression was specifically and significantly up-regulated in TB patients by verification of external data. Gene Ontology functional enrichment analysis and co-expression network showed up-regulated mRNA was mainly involved in negative regulation of the G protein-coupled receptor (GPCR) signaling pathway, and FPR1 and CYP27B1 were involved in the co-expression of AC007128.1. Using the 1000 Genomes Project, software Haploview V4.2, and SNP genotype, we screened out SNP rs12333784 which locus at 7p21.3 in AC007128.1 associated with TB susceptibility. The G carrier of rs12333784 was then finally verified to be significantly associated with pulmonary TB (PTB) and extrapulmonary tuberculosis (EPTB) susceptibility (pBonferroni =0.03878), and a similar but more significant effect was observed under the dominant model analysis (pBonferroni =0.013, OR =1.349, 95% CI, 1.065–1.709). In addition, the GG + GA genotype of SNP rs12333784 was significantly correlated with higher glucose (GLU) (P=0.03), higher gamma-glutamyl transferase (GGT) (P=0.05), and higher erythrocyte sedimentation rate (ESR) (P=0.05).

Our findings show lncRNA AC007128.1 can be regarded as biomarkers discriminating between ATB and LTBI and may also be a diagnostic biomarker for LBTI. These findings may aid clinical decision making in the management of TB.

• AC007128.1
• biomarker
• genetic susceptibility
• single nucleotide polymorphisms (SNPs)
• tuberculosis infection

This study aimed to explore the potential effects of novel non-coding ribose nucleic acids (ncRNAs) in patients with multiple myeloma (MM). The gene expression profile of plasma cells was used for sequence analysis to explore the expression pattern of ncRNAs in MM. The expression patterns of non-coding RNAs in MM were analyzed by RNA sequencing (whole-transcriptome-specific RNA sequencing). Next, the expression of the selected ncRNAs was verified by quantitative real-time polymerase chain reaction. Further, the lncRNA-associated competitive endogenous RNA network in MM was elucidated using deep RNA-seq. Differentially expressed (DE) ncRNAs were significantly regulated in patients with MM. DE target lncRNAs were analyzed by cis and trans targeting prediction. Two new lncRNAs were shown to be related to MM oncogenes. MSTRG.155519 played a carcinogenic role in myeloma by targeting CEACAM1; MSTRG.13132 was related to FAM46C. Finally, the network of lncRNA–mRNA–miRNA in MM was constructed in this study. The expression of non-coding RNAs through sequence and functional analyses might be helpful for further studies on the pathogenesis of MM and the development of new MM-targeted therapy for non-coding RNAs.

• ceRNA
• multiple myeloma
• non-coding RNAs
• oncogene
• sequencing

Majority of the human genome is transcribed to RNAs that do not encode proteins. These non-coding RNAs (ncRNAs) play crucial roles in regulating the initiation and progression of various cancers. Given the importance of the ncRNAs, the roles of ncRNAs in cancers have been reviewed elsewhere. Thus, in this review, we mainly focus on the recent studies of the function, regulatory mechanism and therapeutic potential of the ncRNAs including microRNA (miRNA), long ncRNA (lncRNA), circular RNA (circRNA) and PIWI interacting RNA (piRNA), in different type of cancers.

• cancer
• circular RNA
• long non-coding RNA
• microRNA
• non-coding RNA
• piwi RNA

• Biogenesis
• Biological functions
• CircRNAs
• Clinicopathology
• Diagnosis
• Prognosis
• Regulation mechanisms
• Triple-negative breast cancer

• Animals
• Gene Expression Regulation, Neoplastic
• Humans
• Models, Molecular
• Prognosis
• RNA, Circular/analysis
• RNA, Circular/genetics
• RNA, Circular/metabolism
• Transcriptome
• Triple Negative Breast Neoplasms/diagnosis
• Triple Negative Breast Neoplasms/genetics
• Triple Negative Breast Neoplasms/metabolism

• CRC
• FOXM1
• SMAD3
• miR-4429

• Competing endogenous RNA (CeRNA) network
• Esophageal carcinoma (ESCA)
• molecular biomarker
• series test of cluster analysis

• BCOR
• Laryngeal squamous cell carcinoma
• MIAT
• miR-147a

Non-coding RNA activated by DNA damage (NORAD) has been reported to be a cancer-related long non-coding RNA (lncRNA) implicated in the progression of several cancers; however, its role in breast cancer (BC) has not yet been clarified.

Quantitative real-time polymerase chain reaction was used to examine NORAD, microRNA (miR)-155-5p, and suppressor of cytokine signaling 1 (SOCS1) mRNA expression levels. Western blotting was used to analyze SOCS1 protein expression. The malignancy of BC cells was assessed using the cell counting kit-8 (CCK-8), BrdU, and Transwell assays. Bioinformatics analysis, RNA immunoprecipitation assay, and dual-luciferase reporter gene assays were used to verify the targeted relationship between NORAD and miR-155-5p. Additionally, the regulatory effects of NORAD and miR-155-5p on SOCS1 expression were determined by western blotting.

NORAD expression was significantly reduced in BC cell lines and tissues, and its low expression was associated with poor tumor tissue differentiation. NORAD overexpression repressed BC cell proliferation, migration, and invasion, whereas its knockdown produced the opposite effects. Additionally, miR-155-5p was found to be a target of NORAD, and the biological functions of miR-155-5p and NORAD were counteractive. MiR-155-5p was confirmed to target SOCS1, and SOCS1 was found to be positively regulated by NORAD.

NORAD suppresses miR-155-5p to upregulate SOCS1, thereby repressing the proliferation, migration, and invasion of BC cells.

• Breast neoplasms
• Cell proliferation
• Metastasis

• Cancer
• MIAT
• Myocardial Infarction Associated Transcript
• lncRNA

• Animals
• Apoptosis
• Cell Line, Tumor
• Cell Movement
• Cell Proliferation
• Gene Expression Regulation, Neoplastic
• Heterografts
• Humans
• Neoplasm Invasiveness
• Neoplasm Transplantation
• Neoplasms/genetics
• Neoplasms/metabolism
• Neoplasms/pathology
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Signal Transduction
• Tumor Burden

• ATF3
• Breast cancer
• circRNA
• lncRNA
• miRNA

• Activating Transcription Factor 3/metabolism
• Breast Neoplasms/metabolism
• Cell Line, Tumor
• Computational Biology
• Computer Simulation
• Disease Progression
• Gene Expression Regulation, Neoplastic/physiology
• Humans
• MicroRNAs/metabolism
• RNA, Circular/metabolism
• RNA, Long Noncoding/metabolism

Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown.

LINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis.

LINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p.

LINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.

• Breast cancer
• CTNNB1
• LINC00665
• miR-3619-5p
• β-Catenin

• Breast cancer
• Competing endogenous RNA
• Long non-coding RNA SNHG3
• Notch signaling pathway
• microRNA-154-3p

• Animals
• Breast Neoplasms/metabolism
• Breast Neoplasms/pathology
• Cell Movement/genetics
• Cell Proliferation/genetics
• Female
• Gene Expression Regulation, Neoplastic
• Gene Silencing
• Humans
• MCF-7 Cells
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs/metabolism
• Neoplasm Invasiveness/genetics
• Neoplasm Metastasis/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• RNA, Small Interfering/genetics
• Receptor, Notch2/metabolism
• Signal Transduction/genetics
• Tumor Burden/genetics
• Xenograft Model Antitumor Assays

• bioinformatics analysis
• biomarkers
• breast cancer
• cancer epigenetics
• gene expression
• lncRNAs
• prognosis
• qRT-PCR

• Breast cancer
• DLG3
• Epithelial-to-mesenchymal transition
• Hippo signaling pathway
• LncRNA MIAT
• Lymph node metastasis

• Biomarker
• Cancer
• LncRNA
• MIAT

• ESCC
• FOXP4
• FOXP4-AS1
• IGF2BP2
• proliferation

• EMT
• MIAT
• Melanoma
• miR-150

Accumulating evidence has demonstrated that long non‐coding RNAs (lncRNAs) MIAT is significantly upregulated in many cancer types including gastric cancer (GC). However, the potential clinical significance of serum exosomal MIAT in GC is unknown.

In this study, a total of 109 GC patients, 48 gastric adenoma patients, and 50 healthy individuals were recruited. Serum exosomal MIAT levels were detected in all participants using quantitative real‐time reverse transcription‐polymerase chain reaction (qRT‐PCR).

The exosomes we extracted from the serum samples were positive for TSG101, CD63, and Flotillin‐1, which were known exosome markers. Serum exosomal MIAT levels were significantly higher in GC patients than in gastric adenoma patients and healthy controls. Interestingly, gastric adenoma patients with higher serum exosomal MIAT expression were more prone to develop GC. In addition, serum exosomal MIAT levels were significantly decreased in post‐treatment blood samples compared to pre‐treatment samples, while markedly increased in the cases suffering recurrence. Moreover, serum exosomal MIAT upregulation was significantly associated with worse clinical variables and shorter survival. Furthermore, serum exosomal MIAT was identified as an independent prognostic factor for GC.

Collectively, serum exosomal lncRNA MIAT might serve as a promising novel biomarker for monitoring the progression of GC.

• LncRNA MIAT
• diagnosis
• gastric cancer
• prognosis

Paclitaxel (PTX) is one of the widely used chemotherapy drugs in breast cancer (BC) treatment. Unfortunately, the survival rate of metastatic BC patients remains poor due to PTX resistance. Therefore, uncovering the underlying mechanism behind the PTX resistance of BC cells is crucial for BC therapy.

The enrichment of circular RNA ATP binding cassette subfamily B member 10 (circ-ABCB10), let-7a-5p and dual specificity phosphatase 7 (DUSP7) was measured by quantitative real time polymerase chain reaction (qRT-PCR) in PTX-resistant and PTX-sensitive BC tissues and cells. Chemoresistance, apoptosis, invasion and autophagy of BC cells were measured by 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, transwell invasion assay and Western blot assay, respectively. The binding sites between let-7a-5p and circ-ABCB10 or DUSP7 were predicted by Starbase bioinformatic software, and the combination was confirmed by dual-luciferase reporter assay. The protein expression of DUSP7 was examined by Western blot assay. Murine xenograft model was established to confirm the role of circ-ABCB10 in vivo.

Circ-ABCB10 depletion promoted the PTX sensitivity and apoptosis while suppressed the invasion and autophagy of PTX-resistant BC cells. Circ-ABCB10 could bind to let-7a-5p in BC cells, and circ-ABCB10 contributed to PTX resistance of BC cells via let-7a-5p. DUSP7 is a direct target of let-7a-5p in BC cells, and the accumulation of DUSP7 reversed the promoting effects of let-7a-5p overexpression on the PTX sensitivity and apoptosis and the inhibitory impact on the invasion and autophagy of PTX-resistant BC cells. Circ-ABCB10 interference suppressed the growth of BC tumors in vivo.

Circ-ABCB10 mediated PTX resistance, apoptosis, invasion and autophagy of BC cells via let-7a-5p/DUSP7 axis.

• DUSP7
• breast cancer
• chemoresistance
• circ-ABCB10
• let-7a-5p
• paclitaxel

• breast cancer stem cells
• decitabine resistance
• miR-155
• tetraspanin-5