Identification of differentially expressed miRNAs after overexpression of UBE2CP3 in gastric cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE163814 | GEO | 2021/05/03
REPOSITORIES: GEO
Similar Datasets
Project description:Our data showed that UBE2CP3 was aberrantly upregulated in gastric cancer (GC), but its biofunction in GC is largely unknown to date. To explore the function of lncRNA UBE2CP3 in gastric cancer, loss-of-function and RNA sequencing studies were performed in SGC7901 cell line. The results showed that depletion of UBE2CP3 significantly decreased the expression of ITGA2. Interestingly, ITGA2 was also a target gene of miR-138. Our data showed that UBE2CP3 promotes GC progression through regulating miR-138/ITGA2 axis. Additionally, lncRNA UBE2CP3 could be stabilized by IGFBP7 mRNA. IGFBP7 depletion also significantly decreased ITGA2 expression.
2021-05-03 | GSE163813 | GEO
Project description:Our data showed that EIF4EBP1, NINJ1, CLIC3, STMN3, SPINK4, CD44, GSN, PRSS23 et al. were strongly downregulated by miR-138-mimics in gastric cancer (GC) cell lines. Besides, miR-138-5p has a profound effect on EMT signaling and proliferation signaling. In the EMT signaling, miR-138-5p negatively regulates the expression of SOX4, VIM, TGFB1, BMP1, ECM1 and CXCL8; In the cell proliferation signaling, miR-138-5p could negatively regulates the expression of PCNA, RHOC and CCND3.
2021-10-08 | GSE183654 | GEO
Project description:Circular (circ) RNAs have been widely reported to be involved in gastric cancer (GC) pathogenesis and coiled coil domain containing 6 (CCDC6) is recognized as fused partner of multiple oncogenes; however, the underlying mechanisms of how circRNAs regulate CCDC6 expression in the progression and prognosis of GC remain unclear. Here, we discovered a novel circRNA derived from the DNA2 gene locus (circDNA2) through joint analysis of circRNA microarrays. By performing qRT-PCR and FISH assays with a human tissue microarray, circDNA2 was identified to be highly expressed in GC tissues and associated with lymphatic invasion of GC patients. Knockdown of circDNA2 suppressed the proliferation of GC cells by reducing CCDC6 expression in vitro. Mechanically, circDNA2 acted as a sponge for microRNA (miR)-149-5p, which was validated to target CCDC6 by dual luciferase reporter assays and rescue experiments. Both miR-149-5p low expression and CCDC6 high expression were related to unfavorable prognosis of GC patients. Moreover, GC patients with low miR-149-5p expression had shorter overall survival and higher risk of chemotherapy resistance compared with these with high miR-149-5p expression. In summary, our findings reveal that circDNA2 contributes to the growth and lymphatic metastasis of GC through upregulating CCDC6 expression via sponging miR-149-5p. The circDNA2/miR-149-5p/CCDC6 axis might be developed as a therapeutic target and prognostic indicator for GC patients.
2024-02-25 | GSE167512 | GEO
Project description:MiRNAs regulate posttranscriptional gene expression and are widely implicated in the pathogenesis of complex diseases. We aim to elucidate miRNA regulation of the atrial mRNA signatures that associate with AF. This may provide novel mechanistical insights and candidate targets for therapies using miRNA mimics or antimiRs.
We present combined miRNAs-mRNAs sequencing in atrial tissues of patient without AF (n=22), with paroxysmal AF (n=22) and with persistent AF (n=20). MiRNA and mRNA signatures followed an ordinal scale from nonAF to paroxysmal to persistent AF patients. The previously reported mRNA sequencing identified 5228 differentially expressed genes involved in epithelial to mesenchymal transition, endothelial cell proliferation and extracellular matrix remodelling involving collagens, glycoproteins and proteoglycans. We discovered 103 differentially expressed miRNAs. Key downregulated miRNAs included miR-135b-5p, miR-138-5p, miR-200a-3p, miR-200b-3p and miR-31-5p and key upregulated miRNAs were miR-144-3p, miR-15b-3p, miR-182-5p miR-18b-5p, miR-4306 and miR-206. The expression levels of differentially expressed miRNAs were negatively correlated with the expression levels of their predicted target mRNAs. The downregulated miRNAs demonstrated a more profound transcriptome effect than the upregulated miRNAs. Upregulated biological processes enriched in miRNAs targets related to epithelial and endothelial cell migration and glycosaminoglycan biosynthesis, in line with the processes discovered by the mRNA sequencing analysis.
Combined analysis of miRNA and mRNA sequencing uncovered miRNAs with a broad transcriptional effect in human AF. Epithelial to mesenchymal transition and endothelial cell proliferation were processes controlled by downregulated miR-135b-5p, miR-138-5p, miR-200a-3p, miR-200b-3p and miR-31-5p, which in turn may contribute to (myo)fibroblast activation and structural remodeling.\
| EGAS00001005296 | EGA
Project description:In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and ELF3-AS1 in gastric cancer. The results showed that lncRNA ELF3-AS1 knockdown decreased the expression of miR-33a/b and miR-203a. Due to miR-33a/b and miR-203a were able to target SNAI2 expression, and ELF3-AS1 knockdown significantly upregulates SNAI2 expression, we speculated ELF3-AS1 may negatively regulate SNAI2 expression through positively regulating the expression of miR-33a/b and miR-203a in GC.
2021-10-01 | GSE161553 | GEO
Project description:The contribution of microRNA-mediated posttranscriptional regulation on the final proteome in differentiating cells remains elusive. Here, we evaluated the impact of microRNAs (miRNAs) on the proteome of human umbilical cord blood-derived unrestricted somatic stem cells (USSC) during retinoic acid (RA) differentiation by a systemic approach using next generation sequencing analysing mRNA and miRNA expression and quantitative mass spectrometry-based proteome analyses. Interestingly, regulation of mRNAs and their dedicated proteins highly correlated during RA-incubation. Additionally, RA-induced USSC demonstrated a clear separation from native USSC thereby shifting from a proliferating to a metabolic phenotype. Bioinformatic integration of up- and downregulated miRNAs and proteins initially implied a strong impact of the miRNome on the XXL-USSC proteome. However, quantitative proteome analysis of the miRNA contribution on the final proteome after ectopic overexpression of downregulated miR-27a-5p and miR-221-5p or inhibition of upregulated miR-34a-5p, respectively, followed by RA-induction revealed only minor proportions of differentially abundant proteins. In addition, only small overlaps of these regulated proteins with inversely abundant proteins in non-transfected RA-treated USSC were observed. Hence, mRNA transcription rather than miRNA-mediated regulation is the driving force for protein regulation upon RA-incubation, strongly suggesting that miRNAs are fine-tuning regulators rather than active primary switches during RA-induction of USSC.
2020-01-31 | PXD016915 | Pride
Project description:Increasing studies report that miR-194-5p plays a tumor suppressor role in gastric cancer (GC). Previous studies have revealed that miR-194 inhibited gastric cancer progression through different pathways by affecting the expression level of different target genes. For example, miR-194 have been reported to be able to regulate the expression of FOXM1, NR2F2, BMI1, SDAD1, RBX1, KDM5B, ZEB1 and AKT2 etc. It suggested that miR-194 may play complicated roles in GC. To figure out the mechanism of miR-194' tumor suppressor role in GC, we performed RNA sequencing in two different GC cell lines. Our studies showed that miR-194 tends to regulated target genes by binding on their 3' untranslated regions with either 7-mer-A1 or 7-mer-m8 or 8-mer. Approximately 138 genes were downregulated in both SGC7901 and BGC823 cell lines that transfected with miR-194-5p mimics compared to negative control siRNAs. Most of the downregulated genes have not reported yet.
2019-10-01 | GSE134308 | GEO
Project description:In order to identify the targets of miR-193a-5p in osteosarcoma U2OS cell line, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins. order to identify the targets of miR-193a-5p, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins.
2021-09-08 | PXD013987 | Pride
Project description:The aim of this study was to identify and evaluate exosomal miRNAs in serum as early diagnostic markers for gastric cancer (GC). Methods: Using next-generation sequencing (NGS) and bioinformatics, we identified candidate serum exosomal miRNA markers for early detection of GC in patients. The candidates were further validated by qRT-PCR in 50 newly recruited early-stage GC patients and matched healthy individuals. Results: NGS revealed that the average mappable reads in the RNA libraries were about 6.5 million per patient. A total of 66 up and 13 down-regulated exosomal miRNAs were found in the screened cohort after removal of log2 transformed read counts <5 and p >0.05. In the validation cohort, by comparing candidate exosomal miRNAs levels in early-stage GC patients and healthy individuals, higher levels of miR-92b-3p, let-7g-5p, miR-146b-5p and miR-9-5p were found to be significantly associated with GC. Diagnostic power of the combined panels of the exosomal miRNAs or the combination of exosomal miRNAs and CEA outperformed that of single exosomal miRNA marker for establishing a diagnosis of early-stage GC. In addition, serum levels of exosomal miR-92b-3p were significantly associated with low adhesion, let-7g-5p and miR-146b-5p were significantly correlated with nerve infiltration, and miR146b-5p was statistically correlated with tumor invasion depth in early-stage GC. Conclusions: Serum exosomal miR-92b-3p, -146b-5p, -9-5p, and let-7g-5p may serve as potential noninvasive biomarkers for early diagnosis of GC. Further validation of these candidate exosomal miRNAs in larger experimental cohorts are required in order to confirm the diagnostic values.
2020-02-21 | GSE130654 | GEO
Project description:Lung cancer is an intrinsically highly metastatic disease and the leading cause of cancer-related deaths worldwide. Although discovery of molecular aberrations in lung adenocarcinomas has led to development of effective targeted therapies, corresponding “drivers” in lung squamous carcinomas (LUSC) have not materialized. Extensive molecular profiling has revealed LUSC tumors have non-recurrent somatic mutations and are largely driven by copy number alterations. Because microRNAs (miRs) play increasingly important roles in regulating metastasis-relevant pathways, we evaluated whether miRs can regulate LUSC progression. By integrating bioinformatics of the Cancer Genome Atlas (TCGA) with novel, highly metastatic LUSC models, we found that miR-671-5p is a key inhibitor of LUSC metastasis. Surprisingly, miR-671-5p regulates LUSC metastasis by inhibiting a circular RNA (circRNA), CDR1as. Although the putative function of CDR1as is through miR-7 sponging, we found miR-671-5p more potently silences an axis of CDR1as and its anti-sense transcript, cerebellar degeneration related antigen 1 (CDR1). To our knowledge, no function of CDR1 has ever been described. We found loss of CDR1as and CDR1 significantly inhibited LUSC metastases. Intriguingly, CDR1 was strongly associated with an epithelial-mesenchymal transition (EMT) program in LUSC tumors, and was sufficient to promote metastases, increased migration and substrate-independent survival, known as anoikis-resistance. CDR1, which directly interacts with AP1 and COPI subunits, no longer promoted migration and anoikis-resistance upon blockade of Golgi trafficking. Our findings reveal a miR/circRNA axis that regulates LUSC metastases through an enigmatic protein, CDR1.
2021-09-08 | PXD012286 | Pride