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Guangsangon E triggers mitochondria dysfunction and mitophagy in triple-negative breast cancer and leads to non-apoptotic cell death
Molecular Carcinogenesis ( IF 4.6 ) Pub Date : 2022-09-19 , DOI: 10.1002/mc.23463
Yuhang Shen 1, 2 , Zhuo Han 1 , Luping Wang 1, 2 , Yan Liang 1, 3 , Xiaoyong Zhang 1, 2 , Wei Li 1, 2 , Shouxin Li 1 , Jingkui Tian 1 , Haote Han 1
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Guangsangon E (GSE) is a natural product separated from Morus alba L. It has been reported to treat lung cancer through autophagy. However, whether GSE is effective in repressing triple-negative breast cancer (TNBC) cells is yet to be elucidated. In the present study, GSE inhibited cell growth of MDA-MB-231, MDA-MB-453, and MDA-MB-468 cells. Moreover, GSE induced mitochondrial dysfunction, including membrane potential loss, mitochondria fission, and reactive oxygen species accumulation, and finally led to mitophagy-related non-apoptotic cell death. In the xenograft tumor nude mice, GSE treatment significantly reduced the size and weight of MDA-MB-231 tumors. The tumor inhibition rates of GSE treatment were 49.68% (low-dose) and 48.73% (high-dose). In summary, GSE is a potential anticancer drug available for treating TNBC with apoptosis resistance.

中文翻译:

光三宫 E 引发三阴性乳腺癌线粒体功能障碍和线粒体自噬,导致非凋亡性细胞死亡

Guangsangon E (GSE) 是从桑树中分离出来的天然产物L. 据报道通过细胞自噬治疗肺癌。然而,GSE 是否能有效抑制三阴性乳腺癌 (TNBC) 细胞还有待阐明。在本研究中,GSE 抑制 MDA-MB-231、MDA-MB-453 和 MDA-MB-468 细胞的生长。此外,GSE 诱导线粒体功能障碍,包括膜电位丧失、线粒体裂变和活性氧积累,最终导致线粒体自噬相关的非凋亡性细胞死亡。在异种移植肿瘤裸鼠中,GSE 治疗显着减小了 MDA-MB-231 肿瘤的大小和重量。GSE治疗的肿瘤抑制率分别为49.68%(低剂量)和48.73%(高剂量)。总之,GSE 是一种潜在的抗癌药物,可用于治疗具有凋亡抗性的 TNBC。
更新日期:2022-09-19
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