Erratum: Involvement of the Mitochondrial Pathway in p53-Independent Apoptosis Induced by <i>p28GANK</i> Knockdown in Hep3B Cells

It is well known that <i>TP53</i> may mediate apoptosis triggered by anticancer drugs. However, accumulating evidence indicates that <i>TP53</i> may be inactivated by mutations and/or deletions in about 50% of human cancers and, as such, may lead to pronounced resistance to therapeutic agents. Thus, the development of new approaches to improve the efficiency of therapeutic agents in cancer cells harboring mutant <i>TP53</i> may have a significant impact on cancer treatment. It has been reported that knockdown by RNA interference (RNAi) of <i>p28GANK</i> (an alias of the gene <i>PSMD10</i>), a novel oncogene over-expressed in hepatocellular carcinoma (HCC), can induce apoptosis in HepG2, a <i>TP53</i>-intact HCC cell line. Because of the high frequency <i>TP53</i> mutations in HCC, it is relevant to know whether <i>p28GANK</i> knockdown-induced apoptosis is also operational in <i>TP53</i>-negative HCC cells. Here, we investigated Adsi<i>p28GANK</i>-induced apoptosis in the <i>TP53</i>-negative HCC cell line Hep3B. Our results indicate that <i>p28GANK</i>-knockdown induces the generation of reactive oxygen species (ROS), which in turn activates p38. Since p38 can signal to Bax, its activation may lead to mitochondrial transmembrane potential (Δψm) loss, cytochrome c release from mitochondria to cytosol, and caspase-9 activation, eventually triggering the mitochondrial pathway of apoptosis.