Nexrutine inhibits cancer cell growth as a consequence of mitochondrial damage and mitophagy
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Updated: Apr 11, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Xiang Wu1, Shao-Ming Zhou, Yi-Ling Ding
1Department of Obstetrics and Gynecology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background/Aims:
Nexrutine is an herbal extract of Phellodendron amurense and has been used as nutrient supplement in China as well as America. Potential protection effect of Nexrutine has been reported.
Methods:
To investigate the mechanism of Nexrutine, we used the HeLa, U2OS and HCT116 as a model. Based on the acidification of cell culture media, we examined the lactate, mitochondria damage as well as mitophagy status by corresponding assay.
Results:
Our data suggest that Nexrutine alters the cellular glucose metabolism to promote lactate production. This effect is caused by mitochondrial damage, not an alteration to lactate dehydrogenase activity. As a result of the mitochondrial damage, cell proliferation was inhibited and was associated with an elevation in p21/p27 proteins, which are both important cell cycle inhibitors. As another consequence of the mitochondrial damage, mitophagy was highly activated in Nexrutine-treated cells in a dose-dependent manner. When the autophagy pathway was blocked by siRNAs against BECN1 or ATG7, the growth inhibition caused by Nexrutine was reversed.
Conclusion:
Our study revealed that autophagy plays an important role in the inhibition of cancer cell proliferation by Nexrutine.
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