Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA271485 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Pseudogene INTS6P1 regulates its cognate gene INTS6 through competitive binding of miR-17-5p in hepatocellular carcinoma
| PRJNA271483 | ENA
Project description:Pseudogene INTS6P1 regulates its cognate gene INTS6 through competitive binding of miR-17-5p in hepatocellular carcinoma [mRNA, lncRNA]
| PRJNA271486 | ENA
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR. RNA was extracted from 3 pairs of HCC and normal liver tissue harvested from patients to undergo microarray study.
2015-01-03 | E-GEOD-64631 | biostudies-arrayexpress
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR. RNA was extracted from 3 pairs of HCC and normal liver tissue harvested from patients to undergo microarray study.
2015-01-03 | E-GEOD-64632 | biostudies-arrayexpress
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR.
2015-01-03 | GSE64632 | GEO
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR.
2015-01-03 | GSE64631 | GEO
Project description:Intervertebral disc (IVD) herniation is a complex and multifactorial condition with challenging diagnosis and limited therapeutic options, highlighting the need for reliable biomarkers to improve clinical decision-making. The aim of this study was to identify circulating prognostic biomarkers of IVD herniation regression. The plasma proteomic profile and the expression of circulating non-coding RNAs wereas analysed in a rat model ofs subjected to IVD herniation and proteomic and miRNA levels were correlated to herni-ation size. Four candidate proteins were identified (TNC, COPS3, JUP, GNAI2) that were significantly correlated with herniation size, with TNC further validated by ELISA. Additionally, miR-143-3p, miR-10b-5p, miR-27a-3p, miR-140-5p, miR-155-5p, miR-146a-5p and miR-21-5p were positively correlated with herniation size. Moreover, TNC, COPS3, JUP and GNAI2 were found to be potentiala targets of miR-155-5p. TNC-miR-155-5p pro-tein-miRNA pair standout as promising candidates to be part of a putative regulatory module worth investigating as a prognostic tool. This study provides the first combined proteomic and miRNAs account of preclinical plasma biomarkers of IVD herniation size, where TNC-miR-155-5p emerge as promising elements of a regulatory module with IVD herniation prognostic potential.
2026-02-02 | PXD071649 | Pride
Project description:Abstract Objectives: Abdominal aortic aneurysm (AAA) is a fatal cardiovascular disease with no effective drug treatment currently available. The aberrant expressions of microRNAs (miRNAs) contribute to AAA pathogenesis. In this study, we aimed to perform miRNA microarray analysis to screen for differentially expressed miRNAs in the aortas of AAA mice compared to those in control mice, and to clarify the role and mechanism of miRNA-378a-5p (miR-378a-5p) in the AAA development. Methods: We performed a comprehensive miRNA microarray analysis to screen for differentially expressed miRNAs in the aortas of AAA mice and control mice. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-378a-5p in the serum and aortas of AAA patients and mice. To clarify the role of miR-378a-5p in the AAA development in vivo, miR-378a-5p antagomir and angomir were administered to ApoE-/- mice using tail venous injection, followed by Angiotensin II (Ang II) infusion. Next, the role of miR-378a-5p in the phenotypic switching and migration of vascular smooth muscle cells (VSMCs) was examined in vivo and in vitro. Mechanistically, the targets of miR-378a-5p were identified by bioinformatics analysis, luciferase assay, qRT-PCR and western blot. Co-immunoprecipitation (Co-IP) assay combined with mass spectrometry were carried out for excavating potential downstream effectors. Results: The expression of miR-378a-5p was decreased in the serum and aortas of AAA patients and mice, and tumor necrosis factor-α (TNFα)-treated VSMCs. In vivo, the antagomir-378a-5p aggravated AAA formation, as evidenced by a larger maximal aortic diameter and greater medial elastin degradation than in control mice. MiR-378a-5p angomir had the opposite effect. In vitro, miR-378a-5p overexpression significantly promoted the contraction ability and suppressed the migration of VSMCs, whereas miR-378a-5p knockdown inhibited the contraction ability and increased the migration of VSMCs. Mechanistically, we discovered that miR-378a-5p played a protective role in AAA development by regulating actin-binding LIM protein 1 (ABLIM1)-megakaryoblastic leukemia 1 (MKL1) pathway. Conclusion: MiR-378a-5p exerts protective effects against AAA by maintaining VSMCs homeostasis via the ABLIM1-MKL1 pathway. Therefore, targeting miR-378a-5p may be an attractive therapeutic strategy for AAA treatment.
2026-01-13 | PXD073033 |
Project description:Post-transcriptional regulation of gene expression by miRNAs likely makes significant contributions to mRNA abundance at the embryo-maternal interface. In this study, we investigated how miR-26a-5p and miR-125b-5p contribute to molecular changes occurring in the uterine luminal epithelium, which serves as the first site of signal exchange between the mother and developing embryo. To measure de novo protein synthesis after miRNA delivery to primary uterine luminal epithelial cells, we employed pulsed stable isotope labeling by amino acids (pSILAC). We found that both miRNAs alter the proteome of luminal epithelial cells, impacting numerous cellular functions, immune responses, as well as intracellular and second messenger signaling pathways. Additionally, we identified several features of miRNA-mRNA interactions that may influence the targeting efficiency of miR-26a-5p and miR-125b-5p. Overall, our study suggests a complex interaction of miR-26a-5p and miR-125b-5p with their respective targets. However, both appear to cooperatively function in modulating the cellular environment of the luminal epithelium, facilitating the morphological and molecular changes that occur during the intensive communication between the embryo and uterus at pregnancy.
2025-05-07 | PXD056243 | Pride
Project description:Hepatocellular carcinoma (HCC) remains a significant clinical challenge due to limited diagnostic and therapeutic options. Non-coding RNAs, such as microRNAs (miRNAs), play key roles in cancer biology. Our previous findings showed that miR-423-5p exerts anti-cancer effects on HCC patients treated with sorafenib by promoting autophagy. In this study, we investigated the molecular mechanisms underlying its activity by generating SNU-387 HCC cell line stably overexpressing miR-423-5p and conducting a comprehensive proteomic analysis. Mass spectrometry profiling identified 698 differentially expressed proteins (DEPs) in miR-423-5p-overexpressing cells compared to controls. Functional enrichment analysis revealed significant alterations in metabolic pathways, particularly purine/pyrimidine metabolism and gluconeogenesis. To relate these findings to clinical context, we integrated experimentally validated and predicted miR-423-5p targets with The Cancer Genome Atlas (TCGA) Liver Hepatocellular Carcinoma (LIHC) dataset. Seven candidate proteins were significantly associated with patient prognosis (log-rank p < 0.05 for both overall and disease-free survival). These targets were downregulated in our miR-423-5p model but found to be upregulated in stage III HCC tissues from TCGA data.
2025-09-29 | PXD064869 | Pride