Guangsangon E triggers mitochondria dysfunction and mitophagy in triple-negative breast cancer and leads to non-apoptotic cell death

  • Mol Carcinog. 2022 Sep 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
Affiliations
  • 1. The Cancer Hospital of the University of Chinese Academy of Science (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Science, Hangzhou, Zhejiang, China.
  • 2. Department of Biomedical Engineering, College of Biomedical Engineering & Instrument Science, Zhejiang University, Hangzhou, China.
  • 3. Department of Nephrology, Urology & Nephrology Center, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.
PMID: 36121321 DOI: 10.1002/mc.23463
Abstract

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.

Keywords
Guangsangon E; ROS; TNBC; mitochondria dysfunction; mitophagy.
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