Journal
VIROLOGY
Volume 511, Issue -, Pages 1-8Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2017.08.002
Keywords
PTEN-Long; Hepatitis C virus; Viral replication; Core; Protein - protein interaction
Categories
Funding
- Canadian Institutes of Health Research (CIHR) [109427]
- Saskatchewan Health Research Foundation
- Natural Sciences and Engineering Research Council of Canada
- CIHR [NHC-142832]
- Public Health Agency of Canada (PHAC)
- University of Saskatchewan Vaccinology and Immunotherapeutics
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Hepatitis C virus (HCV) infection is a confirmed risk factor for hepatocellular carcinoma (HCC). Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) possesses tumor suppression function that is frequently defective in HCC tumors. PTEN-Long, a translation isoform of PTEN, functions in a cell non-autonomous manner. In this study, we demonstrated that intracellular overexpression of PTEN-Long inhibits HCV replication. More importantly, we showed that treatment with extracellular PTEN-Long protein inhibits HCV replication in a dose-dependent manner. Furthermore, we showed that PTEN-Long interacts with HCV core protein and this interaction is required for HCV replication inhibition by PTEN-Long. In summary, we demonstrated, for the first time, that PTEN-Long protein, an isoform of the canonical PTEN and in the form of extracellular protein treatment, inhibits HCV replication. Our study offers an opportunity for developing additional anti-HCV agents.
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