目的:国内外研究表明,新城疫病毒在体内外对多种肿瘤具有明显抑制作用。本研究旨在探讨新城疫病毒D90株体外对乳腺癌MCF-7细胞的作用及可能机制。方法:CCK-8法检测MCF-7细胞增殖抑制;光学显微镜及DAPI染色观察D90株对MCF-7细胞形态学影响;流式细胞术检测MCF-7细胞凋亡率;Western blot检测MCF-7细胞凋亡相关蛋白的表达情况。结果:D90株对MCF-7细胞具有显著抑制作用并呈浓度和时间依赖性;D90株能够诱导MCF-7细胞凋亡并调节凋亡相关蛋白的表达,包括上调Bax蛋白、下调Bcl-2蛋白,并促进Caspase-3和Caspase-9的裂解活化。结论:D90株能够调节凋亡相关蛋白的表达,并促进Caspase-3和Caspase-9的裂解活化,通过线粒体途径诱导MCF-7细胞凋亡并呈浓度和时间依赖性。 OBJECTIVE: Domestic and foreign studies show that Newcastle disease virus has a significant inhibitory effect on various tumors both in vitro and in vivo. The purpose of this study was to investigate the effect and possible mechanism of Newcastle disease virus D90 strain on breast cancer MCF-7 cells in vitro. Methods: The proliferation of MCF-7 cells was detected by CCK-8 method. The morphological changes of MCF-7 cells were observed by light microscopy and DAPI staining. The apoptosis rate of MCF-7 cells was detected by flow cytometry. Apoptosis-related protein expression. Results: D90 strain could significantly inhibit the proliferation of MCF-7 cells in a concentration-and time-dependent manner. D90 strain could induce the apoptosis of MCF-7 cells and regulate the expression of apoptosis-related proteins, including upregulation of Bax and downregulation of Bcl-2 , And promote the cleavage activation of Caspase-3 and Caspase-9. Conclusion: D90 can regulate the expression of apoptosis-related proteins and promote the activation of Caspase-3 and Caspase-9. Mitochondria induced the apoptosis of MCF-7 cells in a concentration-and time-dependent manner.