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3,5-diCQA suppresses colorectal cancer cell growth through ROS/AMPK/mTOR mediated mitochondrial dysfunction and
Weibing Wang1, Xingwei Xu1, Long Zhao1
1Department of Colorectal and Anal Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Abstract:
3,5-diCQA has been shown to have anti-tumor effect by decreasing cancer cell growth. However, the molecular mechanism by which 3,5-diCQA impacts colorectal cancer (CRC) cells is unknown. This study discovered that 3,5-diCQA had a suppressive effect on CRC cells, mainly in the inhibition of proliferation, migration, and the enhancement of apoptosis in HCT116 and SW480 cells. Additionally, 3,5-diCQA was found to cause cell cycle arrest in CRC cells. Meanwhile, we found that 3,5-diCQA activates the AMPK pathway through the generation of ROS, mediates mitochondrial damage, and reduces mitochondrial aerobic glycolysis and oxidative phosphorylation levels. 3,5-diCQA promoted oxidative damage and ferroptosis in CRC cells. Hence, we added ROS inhibitor NAC and found that the NAC reversed the effects of 3,5-diCQA on proliferation, apoptosis, ROS generation, and ferroptosis in CRC cells. Moreover, 3,5-diCQA was also shown to suppress the development of CRC tumor in a tumor-forming model of nude mice. In conclusion, we found that 3,5-diCQA enhances the oxidative damage and ferroptosis while reducing proliferation and migration of CRC cells, depending on mitochondrial dysfunction caused by the ROS/AMPK/mTOR pathway.
Insights
3,5-diCQA suppresses colorectal cancer (CRC) growth by inducing oxidative damage and ferroptosis. This compound activates the ROS/AMPK/mTOR pathway, leading to mitochondrial dysfunction and reduced proliferation in CRC cells.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Colorectal cancer (CRC) remains a significant global health challenge.
- The anti-tumor effects of 3,5-diCQA are known, but its precise molecular mechanisms in CRC are not fully understood.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying the anti-cancer effects of 3,5-diCQA in colorectal cancer cells.
- To investigate the role of reactive oxygen species (ROS) and the AMPK pathway in 3,5-diCQA's action.
Main Methods:
- Cell proliferation, migration, apoptosis, and cell cycle assays were performed on CRC cell lines (HCT116, SW480).
- Mitochondrial function, including aerobic glycolysis and oxidative phosphorylation, was assessed.
- The involvement of ROS, AMPK pathway, and ferroptosis was investigated, including experiments with ROS inhibitor N-acetylcysteine (NAC).
- In vivo anti-tumor efficacy was evaluated using a tumor-forming model in nude mice.
Main Results:
- 3,5-diCQA significantly inhibited proliferation and migration while enhancing apoptosis and causing cell cycle arrest in CRC cells.
- 3,5-diCQA activated the AMPK pathway via ROS generation, induced mitochondrial damage, and reduced mitochondrial aerobic glycolysis and oxidative phosphorylation.
- The compound promoted oxidative damage and ferroptosis in CRC cells, effects reversed by NAC.
- 3,5-diCQA demonstrated suppressive effects on CRC tumor development in vivo.
Conclusions:
- 3,5-diCQA exerts anti-cancer effects in colorectal cancer by inducing mitochondrial dysfunction through the ROS/AMPK/mTOR pathway.
- This leads to enhanced oxidative damage and ferroptosis, consequently reducing cancer cell proliferation and migration.
- 3,5-diCQA represents a potential therapeutic agent for colorectal cancer treatment.
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