自噬介导葫芦素E对乳腺癌细胞Bcap-37的细胞毒作用

Autophagy is Involved in Anticancer Effects of Cucurbitacin E on Human Breast Cancer Cell Bcap-37

目的研究葫芦素E(Cucurbitacin E,Cu E)或Cu E联合自噬抑制剂氯喹(Chloroquine,CQ)对乳腺癌Bcap-37细胞增殖的影响,并探讨其分子机制。方法 MTT法检测乳腺癌Bcap37细胞增殖抑制作用,流式细胞仪检测细胞凋亡,Western blot检测LC3-Ⅰ/Ⅱ、P62蛋白表达。透射电子显微镜检测自噬溶酶体形成。结果 Cu E通过诱导凋亡显著抑制Bcap-37增殖。经Cu E处理的Bcap-37细胞中自噬特异性标志物LC3-Ⅱ表达增高,而LC3-Ⅰ、P62表达降低。细胞内自噬溶酶体形成。结论 Cu E可诱导Bcap-37细胞凋亡及细胞保护性自噬。抑制自噬可增加Cu E对Bcap-37的细胞毒性。

Objective To explore the effect of Cucurbitacin E（Cu E） or Cu E combined with autophagy inhibitor,Chloroquine（CQ） on the proliferation of human breast cancer cells Bcap-37 and its possible mechanism.Methods MTT assay was used to measure the effect of Cu E or Cu E combined with CQ on Bcap-37 proliferation.The apoptosis was measured by flow cytometry.Western blot was used to detect LC3-Ⅰ/Ⅱand P62 protein expression.The autolysosome was observed by electronic microscopy.Results Cu E significantly inhibited the in vitro growth of human breast cancer cells by inducing the apoptosis.After treated with Cu E,the expression of autophagy-related protein LC3-Ⅱ was increased,while LC3-Ⅰ,P62 expression were decreased.In addition,Cu E also induced the formation of autolysosomes,indicating the activation of autophagy.Conclusion Cu E could induc the apoptosis of human breast cancer cells and cytoprotective autophagy.The inhibition of autophagy could significantly enhance the cytotoxicity of Cu E to Bcap-37.