2. Academic Validation
  3. Guangsangon E triggers mitochondria dysfunction and mitophagy in triple-negative breast cancer and leads to non-apoptotic cell death

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

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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