Secretion clusterin (sClu) is a kind of disease of protein, played an important role in protecting cells from tumor necrosis factor (TNF) α induced apoptosis. The purpose of this study was to survey the molecular mechanism of the influence sClu TNF induced apoptosis in breast cancer cells. The wild type of p53 expression MCF 7 cell line was designed out excessive performance sClu (MCF 7 / sClu), and mda - m - 231 cell line and mutant p53 and sClu son transfection is the silence of the small interference RNA (mda - m - 231 / sClu small interference RNA). Clusterin overexpression influence, in the cell apoptosis and sensitivity are two TNF α in vitro. Our results show that TNF treatment increase BCL 2 mRNA and protein content in breast cancer cells, which suggests that BCL 2 directly subject to nuclear factor - kappaB (NF - kappaB) in response to TNF α. The induction of the base class library 2 mediated p65 subelement of NF - kappaB. The silence of the small interference RNA mediated BCL 2 lead to increased significantly TNF induced apoptosis. The silence of the sClu in mda - m - 231 / sClu small interference RNA cell abolished TNF mediated NF - kappaB activation and BCL 2 overexpression, and present mda - m - 231 / sClu small interference RNA cell significantly more sensitive, TNF than parent mediated apoptosis. In addition, sClu expression in the MCF 7 / sClu cell mediated TNF NF - kappaB promotion activities and BCL 2 overexpression, and presents MCF 7 / Clu cell significant resistance to TNF α mediated apoptosis. Inhibition of NF - kappaB activity or p65 and BCL 2 expression reverse these effects. The results show that sClu awarded breast cancer cells apoptosis induced resistance of TNF α by NF - kappaB activation and BCL 2 overexpression.

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