ArticlePloS one2014
Role of hepatitis C virus induced osteopontin in epithelial to mesenchymal transition, migration and invasion of hepatocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- Epithelial-Mesenchymal Transition Markers in HCVAssociated Hepatocellular Carcinoma: A Multivariate Follow Up Study.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2020Article
- Circulating osteopontin per tumor volume as a prognostic biomarker for resectable intrahepatic cholangiocarcinoma.Hepatobiliary surgery and nutrition · 2019Article
- Article
- The osteopontin-CD44 axis in hepatic cancer stem cells regulates IFN signaling and HCV replication.Scientific reports · 2018Article
- Osteopontin Regulates Hepatitis C Virus (HCV) Replication and Assembly by Interacting with HCV Proteins and Lipid Droplets and by Binding to Receptors αVβ3 and CD44.Journal of virology · 2018Article
- Genotype and genetic variation of HCV infections with low-risk factors in Putian coastal regions, China.Epidemiology and infection · 2017Article
- Tissue expression of β-catenin and E- and N-cadherins in chronic hepatitis C and hepatocellular carcinoma.Archives of medical science : AMS · 2017Article
- Osteopontin regulates the cross-talk between phosphatidylcholine and cholesterol metabolism in mouse liver.Journal of lipid research · 2017Article
- Integrin β4 promotes cell invasion and epithelial-mesenchymal transition through the modulation of Slug expression in hepatocellular carcinoma.Scientific reports · 2017Article
- Osteopontin-A Master Regulator of Epithelial-Mesenchymal Transition.Journal of clinical medicine · 2016Review
- Role of Osteopontin in Liver Diseases.International journal of biological sciences · 2016Review
- Regulation of the metastasis suppressor Nm23-H1 by tumor viruses.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- Epithelial-mesenchymal transition: molecular pathways of hepatitis viruses-induced hepatocellular carcinoma progression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- Hepatitis C virus infection: establishment of chronicity and liver disease progression.EXCLI journal · 2014Review
- Transcription regulation of E-cadherin by zinc finger E-box binding homeobox proteins in solid tumors.BioMed research international · 2014Review
- Article
Corrections and comments
- Retraction · 2019-04-30Concerns/Issues about Data · Duplication of/in Image · Error in Image ·
- Retracted
Authors and funding
6 authors.
Funding
Abstract
Osteopontin (OPN) is a secreted phosphoprotein which has been linked to tumor progression and metastasis in a variety of cancers including hepatocellular carcinoma (HCC). Previous studies have shown that OPN is upregulated during liver injury and inflammation. However, the role of OPN in hepatitis C virus (HCV)-induced liver disease pathogenesis is not known. In this study, we determined the induction of OPN, and then investigated the effect of secreted forms of OPN in epithelial to mesenchymal transition (EMT), migration and invasion of hepatocytes. We show the induction of OPN mRNA and protein expression by HCV-infection. Our results also demonstrate the processing of precursor OPN (75 kDa) into 55 kDa, 42 kDa and 36 kDa forms of OPN in HCV-infected cells. Furthermore, we show the binding of secreted OPN to integrin αVβ3 and CD44 at the cell surface, leading to the activation of downstream cellular kinases such as focal adhesion kinase (FAK), Src, and Akt. Importantly, our results show the reduced expression of epithelial marker (E-cadherin) and induction of mesenchymal marker (N-cadherin) in HCV-infected cells. We also show the migration and invasion of HCV-infected cells using wound healing assay and matrigel coated Boyden chamber. In addition, we demonstrate the activation of above EMT markers, and the critical players involved in OPN-mediated cell signaling cascade using primary human hepatocytes infected with Japanese fulminant hepatitis (JFH)-1 HCV. Taken together, these studies suggest a potential role of OPN in inducing chronic liver disease and HCC associated with chronic HCV infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.