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Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis in colorectal cancer
Chao Wang1,2, Zihao You2, Guoqing Zhou2
1Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Background:
Colorectal cancer (CRC) is one common tumor with the high death rate, and badly affects the normal lives of CRC patients. Amarogentin (AG) has been found to exhibit regulatory roles and join into the progression of multiple diseases. However, the regulatory impacts and associated molecular mechanisms of AG in CRC progression keep unclear.
Methods And Results:
In this study, it was demonstrated that AG weakened CRC cell viability in a concentration- and time-dependent manner. In addition, AG accelerated cell apoptosis by triggering ferroptosis. The cell invasion and EMT process were restrained after AG treatment, but these impacts were reversed after Fer-1 addition. Moreover, it was uncovered that AG retarded Nrf2/HO-1/GPX4 activation. Additionally, AG modulated PTC cell viability and stimulated ferroptosis. At last, it was illustrated that AG suppressed tumor growth in vivo.
Conclusion:
In conclusion, it was disclosed that AG suppressed cell proliferation and EMT process through inducing ferroptosis in CRC, and retarded Nrf2/HO-1/GPX4 activation. This discovery suggested that AG may be one effective drug for ameliorating CRC progression.
Insights
Amarogentin (AG) suppresses colorectal cancer (CRC) cell growth and invasion by inducing ferroptosis and inhibiting the Nrf2/HO-1/GPX4 pathway. This suggests AG may be a potential therapeutic agent for treating CRC.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Colorectal cancer (CRC) presents a significant global health challenge due to its high mortality rate.
- Amarogentin (AG), a compound with known regulatory roles in various diseases, has an unclear mechanism in CRC progression.
Purpose of the Study:
- To investigate the effects and molecular mechanisms of Amarogentin (AG) on colorectal cancer (CRC) progression.
- To determine if AG can suppress CRC cell viability, invasion, and epithelial-mesenchymal transition (EMT).
Main Methods:
- Assessing AG's impact on CRC cell viability, apoptosis, invasion, and EMT in vitro.
- Investigating AG's effect on the Nrf2/HO-1/GPX4 signaling pathway.
- Evaluating AG's efficacy in suppressing tumor growth in vivo.
Main Results:
- AG significantly reduced CRC cell viability, induced apoptosis via ferroptosis, and inhibited cell invasion and EMT.
- AG treatment suppressed the activation of the Nrf2/HO-1/GPX4 pathway.
- AG demonstrated tumor growth suppression in vivo and modulated pancreatic tumor cell (PTC) viability.
Conclusions:
- AG suppresses CRC proliferation and EMT by inducing ferroptosis and inhibiting Nrf2/HO-1/GPX4 activation.
- AG shows potential as an effective therapeutic agent for ameliorating CRC progression.
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