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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

  • 摘要:
    目的 研究葫芦素E(Cucurbitacin E, CuE)或CuE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 CuE通过诱导凋亡显著抑制Bcap-37增殖。经CuE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 CuE可诱导Bcap-37细胞凋亡及细胞保护性自噬。抑制自噬可增加CuE对Bcap-37的细胞毒性。

     

    Abstract:
    Objective To explore the effect of Cucurbitacin E (CuE) or CuE 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 CuE or CuE 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 CuE significantly inhibited the in vitro growth of human breast cancer cells by inducing the apoptosis. After treated with CuE, the expression of autophagy-related protein LC3-Ⅱ was increased, while LC3-Ⅰ, P62 expression were decreased. In addition, CuE also induced the formation of autolysosomes, indicating the activation of autophagy.
    Conclusion CuE could induc the apoptosis of human breast cancer cells and cytoprotective autophagy. The inhibition of autophagy could significantly enhance the cytotoxicity of CuE to Bcap-37.

     

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