title: Inactivated Sendai virus strain Tianjin induces apoptosis in breast cancer MCF-7 cells by promoting caspase activation and Fas/FasL expression.
abstract: Virotherapy represents a promising new approach for treating cancer. Here the authors have analyzed the effect of ultraviolet-inactivated Sendai virus strain Tianjin (UV-Tianjin) on human breast cancer MCF-7 cells in vitro and in vivo. In vitro, UV-Tianjin inhibited the proliferation of MCF-7, MDA-MB-231, and T47D breast cancer cell lines, although MCF-7 cells were most susceptible to UV-Tianjin treatment. Hoechst staining and flow cytometric analysis of UV-Tianjin-treated MCF-7 cells revealed that UV-Tianjin induced apoptosis in a dose-dependent manner. Moreover, UV-Tianjin treatment resulted in reductions in the mitochondria membrane potential of MCF-7 cells and regulated the levels and activities of Bcl-2, Bax, cyt c, caspases, Fas, and Fas ligand (FasL). In vivo, UV-Tianjin inhibited the growth of MCF-7 tumors in nude mice and increased tumor cell apoptosis compared with saline-treated controls. In addition, the percentage of tumor cells positive for cleaved versions of caspase-7, caspase-8, and caspase-9 was higher in UV-Tianjin-treated tumors than in saline-treated controls. In summary, UV-Tianjin exhibited the antitumor activity in human breast cancer MCF-7 cells both in vitro and in vivo. The UV-Tianjin treatment seemed to induce apoptosis by activating both the mitochondrial and death receptor apoptotic pathways.
authors.affiliation: 1 Department of Microbiology, Basic Medical College, Tianjin Medical University , Tianjin, China .
authors.forename: Li-Ying
authors.initials: LY
authors.lastname: Shi
authors.forename: Zhe
authors.initials: Z
authors.lastname: Han
authors.forename: Xiao-Xia
authors.initials: XX
authors.lastname: Li
authors.forename: Mei
authors.initials: M
authors.lastname: Li
authors.forename: Han
authors.initials: H
authors.lastname: Han
authors.forename: Jun
authors.initials: J
authors.lastname: Chen
authors.forename: Sitao
authors.initials: S
authors.lastname: Zang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology / Q000628:therapy* / Q000821:virology; D020169:Caspases / Q000378:metabolism*; D045744:Cell Line, Tumor; D004789:Enzyme Activation; D053222:Fas Ligand Protein / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D061986:MCF-7 Cells; D051379:Mice; D050130:Oncolytic Virotherapy / Q000379:methods*; D029082:Sendai virus / Q000502:physiology*; D038301:Virus Inactivation; D023041:Xenograft Model Antitumor Assays; D019014:fas Receptor / Q000096:biosynthesis*
chemical_list: D053222:Fas Ligand Protein; D019014:fas Receptor; D020169:Caspases
keywords: Sendai virus strain Tianjin; apoptosis; breast cancer cell; caspase; death receptor pathway; mitochondrial pathway