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首页> 外文期刊>Cellular Physiology and Biochemistry >Cantharidin Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing Autophagy and Inducing Apoptosis in Vitro and in Vivo
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Cantharidin Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing Autophagy and Inducing Apoptosis in Vitro and in Vivo

机译：Cantharidin通过抑制自噬并诱导体内和体外凋亡来抑制三阴性乳腺癌细胞的生长。

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>Background/Aims: Cantharidin, a type of terpenoid secreted by the blister beetle Mylabris phalerata (Pallas), has attracted great attention in cancer therapy because of its potential anti-cancer activities. Here, we report the effects on apoptosis and autophagy in human triple-negative breast cancer (TNBC) cell lines after treatment with cantharidin and attempt to elucidate the underlying mechanisms. Methods: MDA-MB-231 and MDA-MB-468 cells were treated with cantharidin and cell proliferation was examined using CCK-8 and clone formation assays. The expression of apoptosis- and autophagy-associated proteins was detected by western blotting. Cells were infected with lentivirus carrying the Beclin-1 gene, and MDA-MB-231-beclin1 (MB231-Bec) and MDA-MB-468-beclin-1(MB468-Bec) cells stably expressing Beclin-1 were established. Autophagic vacuoles in cells were observed with LC3 staining using fluorescence microscopy, and apoptotic cells were detected via flow cytometry. Tumor growth was assessed by subcutaneous inoculation of TNBC cells into BALB/c nude mice. Results: Cantharidin inhibited the proliferation of MDA-MB-231 and MDA-MB-468 cells, and induced cell apoptosis. Cantharidin additionally inhibited the conversion of LC3 I to LC3 II and autophagosome formation by suppressing the expression of Beclin-1. Furthermore, overexpression of Beclin-1 in TNBC cells attenuated the cytotoxicity of cantharidin. In vivo, cantharidin inhibited the growth of MDA-MB-231 and MDA-MB-468 xenografts in nude mice by suppressing autophagy and inducing apoptosis, and Beclin-1 overexpression in TNBC cells reduced the efficacy of cantharidin. Conclusions: Cantharidin inhibits autophagy by suppressing Beclin-1 expression and inducing apoptosis of TNBC cells in vitro and in vivo, thereby representing a potential strategy for the treatment of TNBC.
机译：> 背景/目标： 斑th素（一种由水泡甲虫 Mylabris phalerata （帕拉斯）分泌的萜类化合物）引起了极大的关注。癌症治疗由于其潜在的抗癌活性。在这里，我们报道了用邻苯二酚处理后对人三阴性乳腺癌（TNBC）细胞凋亡和自噬的影响，并试图阐明其潜在机制。 方法： 用角叉素处理MDA-MB-231和MDA-MB-468细胞，并使用CCK-8和克隆形成分析法检测细胞增殖。通过蛋白质印迹检测凋亡和自噬相关蛋白的表达。用携带Beclin-1基因的慢病毒感染细胞，并建立稳定表达Beclin-1的MDA-MB-231-beclin1（MB231-Bec）和MDA-MB-468-beclin-1（MB468-Bec）细胞。使用荧光显微镜通过LC3染色观察细胞中的自噬空泡，并通过流式细胞术检测凋亡细胞。通过将TNBC细胞皮下接种到BALB / c裸鼠中来评估肿瘤的生长。 结果： Cantharidin抑制MDA-MB-231和MDA-MB-468细胞的增殖，并诱导细胞凋亡。 Cantharidin还通过抑制Beclin-1的表达来抑制LC3 I向LC3 II的转化和自噬体的形成。此外，Beclin-1在TNBC细胞中的过表达减弱了邻苯二酚的细胞毒性。 体内，can鱼th素通过抑制自噬和诱导凋亡来抑制裸鼠中MDA-MB-231和MDA-MB-468异种移植的生长，而TNBC细胞中Beclin-1的过表达降低了can鱼th素的功效。 。 结论： 斑th素通过抑制Beclin-1表达并诱导TNBC细胞在体外和体内的凋亡来抑制自噬。 ，因此代表了一种治疗TNBC的潜在策略。

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