Nexrutine Inhibits Cancer Cell Growth as a Consequence of Mitochondrial Damage and Mitophagy

Nexrutine Inhibits Cancer Cell Growth as a Consequence of Mitochondrial Damage and Mitophagy

Blog Article

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 tc m350 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 omni logic plus 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.