| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2167221 | Cellular Immunology | 2011 | 10 Pages |
The retroviral-vector-targeted CD59 gene (pSUPER-siCD59) was constructed and transfected into breast cells (MCF-7). The results demonstrated that the retroviral vector-mediated RNAi successfully suppressed human CD59 gene. The expression of CD59 decreased at both mRNA and protein levels. Knockdown of CD59 abrogated its protective effect on complement-mediated cytolysis. Fas and caspase-3 were remarkably upregulated, which induced apoptosis and tumor growth suppression in MCF-7 cells. In addition, overexpression of CD59 promoted the proliferation of MCF-7 cells and inhibited anti-apoptotic Bcl-2 expression. In conclusion, CD59 may be a promising target in the gene therapy of breast cancer.
► CD59 knockdown inhibit cytolysis. ► CD59 induced MCF-7 apoptosis. ► CD59 overexpression promoted MCF-7 proliferation.
