Clusterin inhibits apoptosis by interacting with activated Bax

Clusterin is a mysterious glycoprotein overexpressed in a variety of human cancers, such as prostate cancer and breast cancer, as well as squamous cell carcinoma1, 2. Since the inhibit clusterin expression presents a sensitive human tumor cells to chemotherapeutic drug-mediated apoptosis, prostate cancer antisense target in clinical trials. However, the molecular mechanism of apoptosis in human cancer cells, inhibition of clusterin is unknown. Here, we report that, tufted cells suppress interference with Bax activation of the mitochondrial apoptosis. Interestingly, the Bax protein inhibitor of clusterin specific interactions conformational change in Bax protein to chemotherapeutic drugs. This interaction hinders: Bax protein oligomerization, resulting in the release of cytochrome c from mitochondria and caspase enzymes activated. In addition, we also found that the profusion inhibit oncogene c-Myc gene mediated apoptosis Bax protein conformational change. Clusterin promoting c-Myc gene mediated, in vitro and in vivo tumor progression. Taken together, the results of our study indicate that elevated levels of clusterin in human cancers may promote oncogenic transformation and tumor progression interference with Bax proapoptotic activities.