[摘要] 目的：探讨GSDME是否通过调控细胞焦亡影响乳腺癌MCF-7 细胞对化疗药物紫杉醇（paclitaxel，PTX）的敏感性。方法：利用RNA干扰技术敲降GSDME在MCF-7 细胞中的表达，采用CCK-8 法、流式细胞术、乳酸脱氢酶（lactate dehydrogenase，LDH）释放实验及Wb技术分别检测GSDME低表达前后，PTX对细胞增殖、焦亡、LDH释放、GSDME-N端蛋白及cleaved-caspase-3 蛋白表达水平的变化情况。结果：与对照组比较，PTX处理组细胞的焦亡率、LDH释放量、GSDME-N端蛋白及cleaved-caspase-3 蛋白的表达水平均显著升高（均P<0.01）；与si-NC组比较，敲低GSDME可使si-GSDME组细胞对PTX的敏感性降低，其细胞焦亡率、LDH释放量及GSDME-N端蛋白表达水平均显著下降（均P<0.01）。结论：敲减MCF-7 细胞中GSDME的表达量可显著抑制细胞焦亡并降低细胞对PTX的敏感性。

[Abstract] Objective: To investigate whether GSDME affects the sensitivity of breast cancer MCF-7 cells to paclitaxel (PTX) by regulating cell pyroptosis. Methods: GSDME was knocked-down in MCF-7 cells by RNA interference technique. CCK-8 assay, flow cytometry,lactate dehydrogenase (LDH) release method and Wb were respectively used to detect cell proliferation, pyroptotic rate, LDH release, GSDME-N-terminal protein and cleaved-caspase-3 protein levels in PTX-treated MCF-7 cells before and after GSDME knockdown.Results: Compared with the control group, the pyroptotic rate, LDH release, GSDME-N-terminal protein and cleaved-caspase-3 protein levels in the PTX-treatment group significantly increased (all P<0.01). Compared with the si-NC group, the PTX-sensitivity of si-GSDME group decreased, and the pyroptotic rate, LDH release and GSDME-N-terminal protein all significantly decreased (all P<0.01). Conclusion: Knock-down of GSDME in MCF-7 cells significantly inhibited cell pyroptosis and reduced drug sensitivity of MCF-7 cells to PTX.

河南省高等学校重点科研计划项目（No. 19A320055）