Abstract
Sendai virus strain Tianjin is a novel genotype. Here, we investigate the antitumor and proapoptotic effects of ultraviolet-inactivated Sendai virus strain Tianjin (UV-Tianjin) on human breast cancer MDA-MB-231 cells in vitro, as well as the involvement of the apoptotic pathway in the mechanism of UV-Tianjin-induced antitumor effects. MTT assays showed that treatment with UV-Tianjin dose-dependently inhibited the proliferation of MDA- MB-231 cells but not normal MCF 10A breast epithelium cells. Hoechst staining and flow cytometric analysis revealed that UV-Tianjin induced apoptosis of MDA-MB-231 cells in a dose-dependent manner. Moreover, UV-Tianjin treatment resulted in reduction in the mitochondria membrane potential (MMP) and release of cytochrome complex (cyt c) via regulation of Bax and Bcl-2, as well as activation of caspase-9, caspase-3, Fas, FasL and caspase-8 in MDA-MB-231 cells. In summary, our study suggests that UV-Tianjin exhibits anticancer activity in human breast cancer MDA-MB-231 cells through inducing apoptosis, which may involve both the endogenous mitochondrial and exogenous death receptor pathways.