Graphene oxide induces autophagy and apoptosis via ROS-dependent AMPK/mTOR/ULK-1 pathway in colorectal cancer cells

Aim: To investigate the anticancer effects and action mechanism of graphene oxide (GO) in colorectal cancer (CRC). Materials & methods: Anticancer effects and mechanisms of GO in CRC were investigated both in vivo and in vitro. Results: GO significantly inhibited tumor growth both in vitro and in vivo. GO was able to enter HCT116 cells through endocytosis. GO treatment resulted in cytotoxicity, reactive oxygen species (ROS) production, apoptosis, autophagy and activation of the AMPK/mTOR/ULK1 signal pathway. However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways. Conclusion: GO exerts anticancer effects against CRC via ROS-dependent AMPK/mTOR/ULK-1 pathway-related autophagy and apoptosis.

Automated summary

This study found that graphene oxide (GO) exhibits anticancer effects against colorectal cancer. GO activates the AMPK/mTOR/ULK1 signaling pathway through the production of reactive oxygen species (ROS), leading to apoptosis and autophagy, thereby inhibiting tumor growth.