{Reference Type}: Journal Article
{Title}: Hepatitis B doubly spliced protein (HBDSP) promotes hepatocellular carcinoma cell apoptosis via ETS1/GATA2/YY1-mediated p53 transcription.
{Author}: Xu X;Zhang L;Ye G;Shi J;Peng Y;Xin F;Lin Y;Wu Q;Lin X;Chen W;
{Journal}: J Virol
{Volume}: 97
{Issue}: 11
{Year}: 2023 Nov 30
{Factor}: 6.549
{DOI}: 10.1128/jvi.01087-23
{Abstract}: <B>OBJECTIVE: </B>Hepatitis B virus (HBV) spliced variants are associated with viral persistence or pathogenicity. Hepatitis B doubly spliced protein (HBDSP), which has been previously reported as a pleiotropic transactivator protein, can potentially serve as an HBV virulence factor. However, the underlying mechanisms of HBDSP in HBV-associated liver diseases remain to be elucidated. In this study, we revealed that HBDSP promotes cellular apoptosis and induces wt-p53-dependent apoptotic signaling pathway in wt-p53 hepatocellular cells by transactivating p53 transcription, and increases the release of HBV progeny. Therefore, HBDSP may promote the HBV particles release through wt-p53-dependent hepatocellular apoptosis. Our findings suggest that blocking HBDSP-induced wt-p53-dependent apoptosis might have therapeutic values for chronic hepatitis B.