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Abstract Title:

Nexrutine inhibits cancer cell growth as a consequence of mitochondrial damage and mitophagy.

Abstract Source:

Cell Physiol Biochem. 2015 ;36(2):763-72. Epub 2015 May 22. PMID: 26021264

Abstract Author(s):

Xiang Wu, Shao-Ming Zhou, Yi-Ling Ding, Ying-Ping Gong, Weiqi Zeng, Yi Cui

Article Affiliation:

Xiang Wu


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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Sayer Ji
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