Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma [patient]

ABSTRACT: Our study identifies TACSTD2 as a novel regulator of two major HCV entry factors, CLDN1 and OCLN, which is strongly downregulated in malignant hepatocytes. These results provide new insights into the complex process of HCV entry into hepatocytes and may assist in the development of more efficient cellular systems for HCV propagation in vitro.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69715 | GEO | 2018/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma [cell line]

Project description:Our study identifies TACSTD2 as a novel regulator of two major HCV entry factors, CLDN1 and OCLN, which is strongly downregulated in malignant hepatocytes. These results provide new insights into the complex process of HCV entry into hepatocytes and may assist in the development of more efficient cellular systems for HCV propagation in vitro.

2018-03-01 | GSE78736 | GEO

Claudin-1 is an Invasion and Metastasis Suppressor of Lung Adenocarcinoma

Project description:Background: Claudin-1(CLDN1), one of the key components of tight junction proteins, was found to be down-regulated in human lung adenocarcinomas. This study we investigated the clinical significance of CLDN1 expression in lung adenocarcinoma patients and its role in cancer progression. Method: CLDN1 mRNA expression was measured in tumor specimens from 51 patients with lung adenocarcinoma. CLDN1 protein expression was also examined by immunohistochemistry on specimens from an independent cohort of 67 lung adenocarcinoma patients. CLDN1 and cancer cell migration, invasion, and in vivo metastasis were studied by compared CLDN1 overexpressed, specific shRNA knockdown cells and controls. The Affymetrix oligonucleotide microarray analysis was performed to identify CLDN1 downstream genes. Results: Lung adenocarcinoma patients with low expression of CLDN1 mRNA had shorter overall survival (p = 0.032, log-rank test). This result was further confirmed by immunohistochemistry of CLDN1 protein expression in an independent cohort of lung adenocarcinoma patients (p=0.024). Over-expression of CLDN1 inhibited lung adenocarcinoma cell migration, invasion, and in vivo metastasis. Knockdown of the exogenous CLDN1 expression in CLDN1 transfectants can restore the cancer cell invasive and metastatic ability. By using Affymetrix microarray we have identified panel of genes altered by CLDN1 over-expression. CLDN1 can up-regulate several cancer invasion/metastasis suppressors such as CTGF, THBS1, DLC1, OCLN, ZO-1, and also down-regulate invasion/metastasis enhancers such as SPP1, CUTL1, TGF-α, SLC2A3, PGF, which support that CLDN1 may behave as an invasion and metastasis suppressor. Conclusions: CLDN is a cancer invasion and metastasis suppressor. CLDN1 expression is a useful prognostic predictor and a potential drug treatment target for lung adenocarcinoma patients. Keywords: genetic modification

2008-12-23 | GSE10309 | GEO

Infection with hepatitis C virus depends on TACSTD2, a regulator of claudin-1 and occludin highly downregulated in hepatocellular carcinoma.

Project description: Not available

| S-EPMC5882150 | biostudies-literature

Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-03-01 | GSE78737 | GEO

Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma

Project description:Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma

| PRJNA313404 | ENA

Epididymal epithelial degeneration and lipid metabolism impairment account for male infertility in occludin knockout mice

Project description:Occludin (OCLN) is a tight junction protein and Ocln deletion mutation causes male infertility in mice. However, the role of OCLN in male reproductive system remains unknown. In this study, we found defective proximal epididymis in Ocln-null mice with impaired sperm motility and fertilization, but no defects in testicular spermatogenesis. Integrative omics analysis revealed the downregulation of gene clusters enriched in acid secretion and fatty acid metabolism in the Ocln-null epididymis, especially the enzymes related to the unsaturated arachidonic acid pathway. The number of proton-pump V-ATPase-expression clear cells, a key player of luminal acidification in the epididymis, declined drastically from prepubertal age before sperm arrival but not in the early postnatal-age. This was accompanied by clear cell apoptosis and increase in pH in the epididymal fluid of OCLN-deficient mice. The lipidomics results showed significantly increased levels of specific DAGs conjugated to unsaturated fatty acids in the Ocln-mutant. Immunofluorescent labeling showed that the arachidonic acid converting enzyme PTGDS and phospholipase PLA2g12a were prominently altered in the principal cells and luminal contents of the Ocln-mutant epididymis. Whereas the carboxylate ester lipase CES1, originally enriched in the WT basal cells, was found upregulated in the Ocln-mutant principal cells. Overall, this study demonstrates that OCLN is essential for maintaining the survival of acid-secreting clear cells and unsaturated fatty acid catabolism in the mouse epididymis, as well as ensuring sperm maturation and male fertility.

2022-11-07 | GSE166141 | GEO

Transcriptome profiles of Huh7.5.1-NTCP cells treated with HBV preS1 peptide

Project description:Chronic hepatitis B, C and D virus (HBV, HCV, HDV) infections are leading causes of liver disease and cancer worldwide. Although these viruses differ markedly in their life cycle and genomic organization, they exclusively infect hepatocytes. Recently, the sodium taurocholate cotransporting polypeptide (NTCP) was identified as the first functional receptor for HBV and HDV. Here, we report that NTCP also facilitates HCV entry into human hepatocytes, by augmenting the bile acid-mediated repression of IFN-stimulated genes (ISGs), including IFITM2 and IFITM3, to increase the susceptibility of cells to HCV entry. Furthermore, an HBV-derived preS1 peptide, known to bind NTCP and to inhibit bile acid uptake and HBV infection, inhibits HCV entry by enhancing the expression of ISGs. Our study highlights NTCP as a novel player linking bile acid metabolism to the interferon response in hepatocytes and establishes a role for NTCP in the entry process of multiple hepatotropic viruses, via distinct mechanisms. Collectively, these findings enhance our understanding of hepatitis virus-host interactions and suggest NTCP as an attractive antiviral target for HBV/HCV co-infection. Transcriptome profiling by DNA microarray of Huh7.5.1 cells transduced to express NTCP.

2016-10-25 | E-GEOD-79089 | biostudies-arrayexpress

Transcriptome profiles of Huh7.5.1-NTCP cells treated with HBV preS1 peptide

2016-10-25 | GSE79089 | GEO

Transcriptome profiles of primary human hepatocytes treated with HBV preS1 peptide with or without bile acids

Project description:Chronic hepatitis B, C and D virus (HBV, HCV, HDV) infections are leading causes of liver disease and cancer worldwide. Although these viruses differ markedly in their life cycle and genomic organization, they exclusively infect hepatocytes. Recently, the sodium taurocholate cotransporting polypeptide (NTCP) was identified as the first functional receptor for HBV and HDV. Here, we report that NTCP also facilitates HCV entry into human hepatocytes, by augmenting the bile acids-mediated repression of IFN-stimulated genes (ISGs), including IFITM2 and IFITM3, to increase the susceptibility of cells to HCV entry. Furthermore, an HBV-derived preS1 peptide, known to bind NTCP and to inhibit bile acids uptake and HBV infection, inhibits HCV entry by enhancing the expression of ISGs. Our study highlights NTCP as a novel player linking bile acids metabolism to the interferon response in hepatocytes and establishes a role for NTCP in the entry process of multiple hepatotropic viruses, via distinct mechanisms. Collectively, these findings enhance our understanding of hepatitis virus-host interactions and suggest NTCP as an attractive antiviral target for HBV/HCV co-infection.

2016-10-25 | GSE85091 | GEO

Tight junction proteins claudin-1 and occludin control hepatitis C virus entry and are downregulated during infection to prevent superinfection.

Project description: Not available

| S-EPMC2643775 | biostudies-literature