β-苦茄碱通过Fas介导的死亡受体途径诱导乳腺癌MCF-7细胞凋亡  

β-Solamarine induces apoptosis in breast cancer MCF-7 cells via the Fas-mediated death receptor pathway

作　　者：苏坤俊 林德安 韦星 SU Kunjun;LIN Dean;WEI Xing(Department of Breast Surgery,Qinzhou Maternal and Child Health Care Hospital,Qinzhou 535000,Guangxi,China;School of Basic Medicine,Youjiang Medical University for Nationalities,Baise 533000,Guangxi,China)

机构地区：[1]广西钦州市妇幼保健院乳腺外科,广西钦州535000 [2]右江民族医学院基础医学院,广西百色533000

出　　处：《右江民族医学院学报》2024年第4期497-502,共6页Journal of Youjiang Medical University for Nationalities

摘　　要：目的探讨β-苦茄碱(Beta-solamarine,BSM)诱导乳腺癌MCF-7细胞凋亡及其对Fas介导的死亡受体途径相关蛋白的影响。方法将不同浓度的BSM对体外培养的乳腺癌MCF-7细胞进行干预。采用MTT法测定细胞增殖抑制率,细胞侵袭试验观察细胞侵袭能力,TUNEL法检测细胞凋亡情况,采用Western Blot对Fas、FADD、Cleaved Caspase-8、Cleaved Caspase-3、Cleaved PARP和PARP蛋白表达水平进行检测。结果BSM处理后的细胞组显示出了较高的抑制率、侵袭细胞数明显下降、细胞凋亡率显著增加,各BSM组的细胞抑制率、侵袭细胞数和凋亡率与正常对照组相比,差异均具有统计学意义(P<0.01)。Caspase-8抑制剂Z-IETD-FMK处理组的细胞凋亡率显著降低,相较于与BSM同剂量组,细胞凋亡率差异具有统计学意义(P<0.01)。在BSM的作用下,MCF-7细胞中Fas、FADD、Cleaved Caspase-8、Cleaved Caspase-3以及Cleaved PARP的表达水平显著提升,而PARP的表达水平下降明显,与正常对照组相比差异均具有统计学意义(P<0.05或P<0.01)。结论BSM在抑制MCF-7细胞的增殖、侵袭和促进细胞凋亡方面显示出显著效果,激活Fas介导的死亡受体途径可能是BSM诱导细胞凋亡的机制之一。Objective To investigate the apoptotic effects ofβ-solamarine(BSM)on breast cancer MCF-7 cells and its effect on proteins associated with the Fas-mediated death receptor pathway.Methods Different concentrations of BSM were used to interfere with breast cancer MCF-7 cells cultured in vitro.The cell proliferation inhibition rate was measured using MTT assay,while cell invasion assay was used to observe cell invasion ability.TUNEL assay was used to detect cell apoptosis.Western blot analysis was employed to detect the expression levels of Fas,FADD,Cleaved Caspase-8,Cleaved Caspase-3,Cleaved PARP,and PARP proteins.Results The cell group treated with BSM showed a higher cell inhibition rate,a significant decrease in the number of invasive cells and a significant increase in cell apoptosis rate,demonstrating statistically difference compared to the normal control group(P<0.01).Treatment with the Caspase-8 inhibitor Z-IETD-FMK group significantly reduced apoptosis rate,demonstrating statistically difference(P<0.01)compared to the BSM-treated group with the same dose.BSM treatment significantly upregulated the expression of Fas,FADD,Cleaved Caspase-8,Cleaved Caspase-3,and Cleaved PARP,while downregulating PARP expression in MCF-7 cells compared to the normal control group,demonstrating statistically difference.(P<0.05 or P<0.01).Conclusion BSM shows significant effects in inhibiting the proliferation,invasion and promoting apoptosis in MCF-7 cells.The activation of the Fas-mediated death receptor pathway appears to be one of the mechanisms through which BSM induces apoptosis.

关 键 词：β-苦茄碱 MCF-7细胞 细胞凋亡 Fas途径 

分 类 号：R737[医药卫生—肿瘤]