Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Research on mechanisms of miR-27a-3p on Cisplatin sensitivity of hepatocellular carcinoma based on next generation sequencing

ABSTRACT: Hepatocellular carcinoma (HCC) accounts for 75% of primary liver cancer, ranking seventh in the incidence rate of tumors worldwide, and second in the mortality rate of tumors. The 5-year survival rate after radical surgery is only 59%-68%, and due to the influence of proliferation, invasion, microvascular infiltration and inflammatory environment of hepatocellular carcinoma, Recurrence is still possible after surgical resection, local ablative therapy or liver transplantation. Systemic antitumor therapy can control disease progression and prolong patient survival, and a variety of kinase inhibitors are used in patients who cannot undergo surgery. However, due to the existence of acquired drug resistance to multikinase inhibitors, its effect is not good. Platinum-based FOLFOX4 is recommended, but its efficacy is limited by drug resistance. miR-27a-3p, located in the short arm of chromosome 19, has been found to be involved in inhibiting the activity, proliferation, angiogenesis, and invasion of liver cancer. Other studies have found that miR-27a-3p regulates the sensitivity of tumors (esophageal cancer and breast cancer) to Cisplatin by regulating the apoptosis of the Bcl-2 protein family. The cells were cultured in DMEM medium supplemented with 10% fetal bovine serum and 1% antibiotic-antimitotic solution. The HCC cell line Huh-7 was transfected using Lipofectamine 3000 reagent following the manufacturer’s protocol and incubated for 48h for further analysis. The gene expression profiles were analyzed of Huh-7 cells transfected with miR-27a-3p mimics or NC to assess effect of miR-27a-3p on Cisplatin sensitivity of HCC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206246 | GEO | 2022/10/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA-27a regulates lipid metabolism and inhibits hepatitis C virus replication in human hepatoma cells

Project description:Gene expression profiling was carried out in Huh-7.5 cells in which miR-27a was over- or under-expressed. Transfection of cells with pre-miR-27a and pre-miR-control, or anti-miR-27a and anti-miR-control enabled down- and up-regulated genes to be determined, respectively. Replication and infectivity of the lipotrophic hepatitis C virus (HCV) is regulated by cellular lipid status. Among differentially expressed micro (mi)RNAs, we found that miR-27a was preferentially expressed in HCV-infected compared with hepatitis B virus (HBV)-infected liver. Gene expression profiling of Huh-7.5 cells showed that miR-27a regulates lipid metabolism by targeting the lipid synthetic transcriptional factor, RXRα, and the lipid transporter, ABCA1 Carrying out a Target Scan (Release 5.2) of miR-27a predicted 921 candidate target genes, and functional gene ontology enrichment analysis of these genes by MetaCore (Thomson Reuters, NY) showed that miR-27a could target the signaling pathways of cytoskeleton remodeling and lipid metabolism . To examine whether these signaling pathways were regulated by miR-27a, gene expression profiling was carried out in Huh-7.5 cells in which miR-27a was over- or under-expressed. Transfection of cells with pre-miR-27a and pre-miR-control, or anti-miR-27a and anti-miR-control enabled down- and up-regulated genes to be determined, respectively. Huh-7.5 cells with miR-27a over- or under-expressed

2013-06-05 | E-GEOD-41737 | biostudies-arrayexpress

MicroRNA-27a regulates lipid metabolism and inhibits hepatitis C virus replication in human hepatoma cells

2013-06-05 | GSE41737 | GEO

Transcriptomic analysis of hepatocellular carcinoma cell lines HepG2 treated with Sorafenib and transfected with miR-200c-3p inhibitor, and miR-222-5p and miR-512-3p mimics

Project description:Hepatocellular carcinoma (HCC) is one of the most common causes of death worldwide and the fourth most prevalent type of cancer. Whereas curative treatments such as liver transplantation, ablation or surgery are optimal for early stages, only paliative treatments are given to intermediate and advanced stages of the disease. Despite the introduction of immune regulators as first-line treatments for advanced stages, Sorafenib is still the standard of care in the clinical practice. In cell lysates, anti-tumoral properties of Sorafenib were related to upregulation of miR-200c-3p (anti-tumoral miRNA) at 6 hours of treatment and downregulation of miR-222-5p and miR-512-3p (pro-tumoral miRNAs) at 24 hours. We have identified these miRNA biomarkers of Sorafenib treatment response in plasma of patients with advanced HCC treated with Sorafenib. In particular, miR-200c-3p has been related to increased survival benefit whereas miR-222-5p and miR-512-3p have been related to worse prognosis. Our study has sequenced HepG2 cells treated with Sorafenib and miR-200c-3p inhibitor, and transfected with miR-222-5p and miR-512-3p mimics to unravel the molecular pathways governing Sorafenib response

2022-04-28 | GSE201695 | GEO

RT-PCR profiling analysis of microRNA expression in cisplatin-resistant cancer

Project description:Chemotherapy remains the primary treatment of advanced solid cancer, including lung cancer. As first line treatment, cisplatin-based therapy is restricted by frequent development of drug resistance. Increasing data showed that programmed cell death protein ligand 1 (PD-L1) plays a vital role in regulating cisplatin resistance. However, the mechanisms underlying are not fully understood. We found miR-526b-3p expression declined while PD-L1 elevated in cisplatin-resistant lung cancer compared to that in cisplatin-sensitive lung cancer by analyzing clinical samples. Importantly, miR-526b-3p was associated with response to cisplatin negatively. We further demonstrated that miR-526b-3p reversed cisplatin resistance, suppressed metastasis, and activated CD8+ T cells in a STAT3/PD-L1-dependent manner. Our findings extended the knowledge of PD-L1-mediated cisplatin resistance of lung cancer. In addition, the introduction of miR-526b-3p provided a new clue to improve the anti-tumor effects of the combination of immunotherapy and chemotherapy. miProfileTM Cancer miRNA qPCR Array

2021-03-12 | GSE168707 | GEO

Identification of differentially expressed microRNAs in liver tissue of Hepatitis B virus (HBV) infected hepatocellular carcinoma (HCC)

Project description:Global expression profiling of miRNAs in liver tissue of HBV infected HCC and chronic hepatitis B (CHB) with no fibrosis was evaluated. A total of 40 differentially expressed miRNAs were identified in HCC. Top 10 miRNAs are validated in more numbers of HCC tisuues by qRT PCR. Finally six miRNAs (miR-15a, miR-16, miR-21,miR-29b-3p, miR-126, miR-142-3p, miR-193a-5p) showed similar expression pattern in both microarray and qRT PCR Differential expression analysis of microRNAs in HBV infected HCC (n=4) compared to CHB patients with no fibrosis (n=8) as control.

2015-04-15 | E-GEOD-67882 | biostudies-arrayexpress

miR-579-3p controls hepatocellular carcinoma formation by regulating the PI3K-AKT pathway in chronically inflamed liver (miRNA expression)

Project description:Background & Aims: Chronic liver inflammation causes continuous liver damage with progressive liver fibrosis and cirrhosis, which may eventually lead to hepatocellular carcinoma (HCC). Whereas, the ten-year incidence for HCC in cirrhotic patients is approximately 20%, many cirrhotic patients remain tumor-free for their entire lives. Therefore, we wanted to clarify the mechanisms defining the different outcomes of chronic liver inflammation. Methods: We designed a longitudinal study comparing the mRNA and miRNA expression profiles in matched non-tumoral liver tissue from patients developing HCC (n = 30) versus patients remaining tumor-free (n = 27). The liver parenchyma was analyzed before and after HCC development in the same patient. Cirrhotic patients remaining tumor-free within a similar time frame served as a control cohort. mRNA expression of genes associated with cancer development and miRNAs were examined by the nCounterNanostring technology. The role of the identified genes involved in HCC development was evaluated by immunohistochemistry and in vitro assays. Results: Comparison of the two cohorts revealed that liver tissue from patients developing HCC displayed activation of NF-B, Insulin receptor and PI3K-AKT pathways, in parallel with increased hepatocyte proliferation and damage. Furthermore, downregulation of miR-579-3p was found as an early step in HCC development. MiR-579-3p directly attenuated PIK3CA expression and consequently AKT and pAKT. In vitro analyses confirmed that miR-579-3p controlled cell proliferation, migration and colony formation. Conclusions: Liver tissues from patients developing HCC revealed a more severe damage to the parenchyma with elevated hepatocyte proliferation. Moreover, miR-579-3p was identified as a potential novel tumor suppressor regulating PI3K-AKT signalling at the early stages of HCC development.

2021-06-20 | GSE116043 | GEO

miR-579-3p controls hepatocellular carcinoma formation by regulating the PI3K-AKT pathway in chronically inflamed liver (mRNA expression)

2021-06-20 | GSE116044 | GEO

MiR-27a-3p in peripheral blood mononuclear cells as a potential marker for pancreatic cancer screening

Project description:Background & Aims: MicroRNAs have been shown to offer great potential in the diagnosis of cancer. We aimed to identify microRNAs in peripheral blood mononuclear cells (PBMCs) for diagnosing pancreatic cancer (PC). Methods: PBMCs microRNA expression was investigated in three independent cohorts including 352 participants (healthy, benign pancreatic/peripancreatic diseases (BPD), and PC). First, we used sequencing technology to identify differentially expressed microRNAs in 60 PBMCs samples for diagnosing PC. Quantitative reverse-transcriptase polymerase chain reaction assay was then applied to evaluate the expression of selected microRNAs. A logistic regression model was constructed using an independent cohort. Area under the receiver operating characteristic curve (AUC) was used to evaluate diagnostic accuracy. Results: We found that PBMCs miR-27a-3p could efficiently discriminate PC from BPD (AUC=0.840; 95% CI, 0.787 to 0.885; sensitivity=82.2%, specificity=76.7%). A panel composed of PBMCs miR-27a-3p and serum CA19-9 provided a high diagnostic accuracy in differentiating PC from BPD in the clinical setting (AUC=0.886; 95% CI, 0.837 to 0.923; sensitivity=85.3%, specificity=81.6%). The satisfactory diagnostic performance of the panel persisted regardless of disease status (AUCs for tumour-node-metastasis stages?,?, and ? were 0.881, 0.884, and 0.893, respectively). Conclusion: PBMCs miR-27a-3p could be a potential marker for PC screening. A panel composed of PBMCs miR-27a-3p and serum CA19-9 has considerable clinical value in diagnosing early-stage PC. Therefore, patients who would have otherwise missed the curative treatment window can benefit from optimal therapy. Examination of different MicroRNA profiles in 3 types of PBMCs samples

2012-05-03 | E-GEOD-37710 | biostudies-arrayexpress

Identification of differentially expressed microRNAs in liver tissue of Hepatitis B virus (HBV) infected hepatocellular carcinoma (HCC)

2015-04-15 | GSE67882 | GEO

Transcriptional changes induced by over-expression of miR-27a-3p in C2C12 myoblasts.

Project description:Skeletal muscle has a central role in whole body metabolism with myofibers that represent its functional units. These are differentiated cells with different contraction power and metabolic traits. Faster contracting myofibers preferentially use glucose as substrate for energy production, while slower use lipids. Myofibers can plastically change phenotypic traits in response to pathophysiological stimuli. Since post-transcriptional mechanisms should administer the changes of these post-mitotic cells, we demonstrated that miR-27a-3p influences myofiber fuel availability and mitochondrial morphology. In vitro and in vivo experiments demonstrate that miR-27a-3p regulates glycogen utilization. We used microarrays to characterize the global changes in gene expression in C2C12 myoblasts due to over-expression of miR-27a-3p.

2019-12-20 | GSE98326 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data