Virendra N Pandey
New Jersey Medical School, USA
Title: Molecular mechanism of tumorigenesis induced by fuse binding protein 1: A potential target for anticancer drug development
Biography
Biography: Virendra N Pandey
Abstract
Persistent Hepatitis C virus (HCV) infection leads to chronic hepatitis C (CHC), which often progresses to liver cirrhosis (LC) and hepatocellular carcinoma (HCC). We recently identified an oncogenic cellular factor, FUSE binding protein 1 (FuBP1), which antagonizes the function of tumor suppressor p53 and promotes persistent HCV replication and associated pathogenesis. We found that the direct target of FuBP1 in cancer cells is the tumor suppressor p53, the function of which is actively suppressed by FuBP1. Knockdown of FuBP1 in cancer cells significantly activates p53, increases their sensitivity to apoptotic stimuli, and drastically reduces cell proliferation and migration. We found that FuBP1 physically interacts with the wild-type p53 as well as all the p53 isoforms found in cancers. FuBP1 interaction with p53 strongly inhibits the target DNA binding function of p53. Mapping of the FuBP1-interaction site on p53 molecule indicated DNA binding domain of p53 as the site of FuBP1 interaction. Since FuBP1 expression is undetectable in normal differentiated cells, its overexpression in most cancers including HCC suggests that it is a potential target for drug development.