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MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells.

ABSTRACT: Deficient DNA repair capacity is associated with genetic lesions accumulation and susceptibility to carcinogenesis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate various cellular pathways including DNA repair. Here we hypothesized that the existence of HBV products may interfere with cellular nucleotide excision repair (NER) through microRNA-mediated gene regulation. We found that NER was impaired in HepG2.2.15 cells, a stable HBV-expressing cell line, compared with its parental cell line HepG2. Altered miRNA expression profile, in particular the significant upregulation of miR-192, was observed in HepG2.2.15 cells. Additionally, ERCC3 and ERCC4, two key factors implicated in NER, were identified as targets of miR-192 and over-expressing miR-192 significantly inhibited cellular NER. These results indicated that persistent HBV infection might trigger NER impairment in part through upregulation of miR-192, which suppressed the levels of ERCC3 and ERCC4. It provides new insight into the effect of chronic HBV infection on NER and genetic instability in cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE27561 | GEO | 2011/08/03

SECONDARY ACCESSION(S): PRJNA138399

REPOSITORIES: GEO

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MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells.

Project description:Deficient DNA repair capacity is associated with genetic lesions accumulation and susceptibility to carcinogenesis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate various cellular pathways including DNA repair. Here we hypothesized that the existence of HBV products may interfere with cellular nucleotide excision repair (NER) through microRNA-mediated gene regulation. We found that NER was impaired in HepG2.2.15 cells, a stable HBV-expressing cell line, compared with its parental cell line HepG2. Altered miRNA expression profile, in particular the significant upregulation of miR-192, was observed in HepG2.2.15 cells. Additionally, ERCC3 and ERCC4, two key factors implicated in NER, were identified as targets of miR-192 and over-expressing miR-192 significantly inhibited cellular NER. These results indicated that persistent HBV infection might trigger NER impairment in part through upregulation of miR-192, which suppressed the levels of ERCC3 and ERCC4. It provides new insight into the effect of chronic HBV infection on NER and genetic instability in cancer. A genome-wide miRNAs microarray was performed to identify differentially expressed miRNAs between HepG2.2.15, a stable HBV-expressing cell line, and its parental cell line HepG2.

2011-08-02 | E-GEOD-27561 | biostudies-arrayexpress

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

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2011-01-14 | E-GEOD-19980 | biostudies-arrayexpress

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

2011-01-14 | GSE19980 | GEO

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Project description:Hepatitis B virus (HBV), belonging to Hepadnaviridae family, remains undetected in early infection and is known to be the cause of several hepatic diseases leading to cirrhosis and hepatocellular carcinoma. We have found that PML-Nuclear Body Speckled 110kDa (Sp110), is hyper-expressed upon HBV infection and intriguingly, Sp110 knock-down significantly reduced viral DNA-load in the culture supernatant of HepG2.2.15 (a HBV expressing cell-line). To understand the molecular basis underlying the viral elimination upon Sp110 silencing in HepG2.2.15 cells, we performed microarray to find the differential transcriptomics in Control siRNA treated vs. Sp110 siRNA treated cells. To understand the molecular basis underlying the viral elimination upon Sp110 silencing in HepG2.2.15 cells, we performed microarray to find the differential transcriptomics in Control siRNA treated vs. Sp110 siRNA treated cells.

2019-08-24 | GSE119072 | GEO

The effects of traditional Chinese medicine Yinqi Sanhuang Jiedu Decoction on gene expression in HepG2.2.15 cells

Project description:Yinqi Sanhuang Jiedu Decoction (YQSHJD) is a clinically-proven formula for treating chronic hepatitis B and related fibrosis, demonstrating significant anti-HBV effects in clinical trials. However, its direct inhibitory effect on HBV and the underlying mechanisms remain unclear. The objective of this study is to elucidate the molecular mechanism through which YQSHJD inhibits HBV. HBV-replicating HepG2.2.15 cells were utilized as an in vitro HBV model to study the impact of YQSHJD on HBV replication. Network pharmacology and transcriptome analysis were used to research the targets for YQSHJD in inhibiting HBV replication. The results showed YQSHJD could inhibit HBV replication through regulation of the host antiviral targets.

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Knockdown of miR-192 and miR-432 in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction

Project description:Small extracellular vesicles (sEVs) play a critical role in cardiac cell therapy by delivering molecular cargo and mediating cellular signaling. Among sEV cargo molecule types, microRNA (miRNA) is particularly potent and highly heterogenous. However, not all miRNAs in sEV are beneficial. Two previous studies utilizing computational modeling identified miR-192-5p and miR-432-5p as potentially deleterious in cardiac function and repair. Here, we show that knocking down miR-192-5p and miR-432-5p in cardiac c-kit+ cell-derived sEVs enhances the therapeutic capabilities of sEVs in vitro and in a rat in vivo model of cardiac ischemia reperfusion. miR-192-5p and miR-432-5p depleted CPC-sEVs enhance cardiac function by reducing fibrosis, enhancing mesenchymal stromal cell-like cell mobilization, and inducing macrophage polarization to the M2 phenotype. Knocking down deleterious miRNAs from sEV could be a promising therapeutic strategy for treatment of chronic myocardial infarction.

2022-12-31 | GSE196469 | GEO

The Co-regulated Genes by Ectopic Expression of MiR-371-372-373 Cluster in HepG2 Cells

Project description:MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate. miR-371-372-373-HepG2 vs. mock-HepG2

2012-01-15 | E-GEOD-19981 | biostudies-arrayexpress

Gene expression signatures for entecavir treated HepG2.2.15 cells compared to entecavir untreated HepG2.2.15 cells

Project description:To further analyze the gene expression profile regulated by entecavir, we employed whole genome microarray expression profiling as a discovery platform to identify the differentially expressed genes. Human hepatocellular carcinoma cell lines HepG2.2.15 cells were treated for 48 hr with 10 μmol/L entecavir or 0μmol/L entecavir(control samples) in vitro. The differentially expressed genes including all detected and normalized signal more than 8 were selected and 30 upregulated- and downregulated- genes were identified between 10μmol/L dose and control samples.Afterwards, the differentially-expressed genes were analyzed using KEGG database (http://www.genome.jp/kegg/) and none of 30 genes were related to HBV infection-related molecular interaction network were identified.

2017-05-24 | GSE81831 | GEO

SGBS adipocytes overexpressing miR-192* or a non-targeting control miRNA

Project description:To determine whether expression microRNAs (miRNAs) in visceral adipose tissue (VAT) is altered in human non-alcoholic fatty liver disease (NAFLD), we first performed miRNA profiling of VAT from subjects with (n=15, macroscopic liver fat >30%) or without (<5%, non-NAFLD, n=15) NAFLD. VAT miRNA expression profiles in the two groups were similar except for a single miRNA, miR-192*, which was 1.9-fold increased in NAFLD. We next overexpressed miR-192* in cultured human adipocytes, measured its effect on the cellular triglyceride content, and characterized these adipocytes by transcriptomic profiling followed by pathway analysis, qPCR and quantification of select cellular proteins.

2014-11-05 | GSE62951 | GEO

Gene expression signatures for TCM Suduxing treated HepG2.2.15 cells compared to Suduxing untreated HepG2.2.15 cells

Project description:To further analyze the gene expression profile regulated by TCM Suduxing, we employed whole genome microarray expression profiling as a discovery platform to identify the differentially expressed genes. Human hepatocellular carcinoma cell lines HepG2.2.15 cells were treated for 48 hr with 0.001 μg/ml and 0.01μg/ml Suduxing or without Suduxing(control samples) in vitro. The differentially expressed genes including all detected and normalized signal more than 8 were selected and 538 upregulated- and downregulated- genes were identified between 0.01μg/ml dose and control samples.Afterwards, the differentially-expressed genes were analyzed using KEGG database (http://www.genome.jp/kegg/) and 10 genes related to HBV infection-related molecular interaction network were identified.

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