1. Academic Validation
  2. Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis in colorectal cancer

Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis in colorectal cancer

  • BMC Gastroenterol. 2025 Jan 30;25(1):46. doi: 10.1186/s12876-025-03649-w.
Chao Wang 1 2 Zihao You 2 Guoqing Zhou 2 Juanjuan Dong 2 Sihao Tong 2 Guoping Sun 3
Affiliations

Affiliations

  • 1 Department of Oncology, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, 230022, China.
  • 2 Department of Oncology, Chaohu Hospital of Anhui Medical University, Chaohu, 238000, China.
  • 3 Department of Oncology, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, 230022, China. aysunguoping@163.com.
Abstract

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.

Keywords

Amarogentin; Colorectal cancer; EMT process; Ferroptosis; Nrf2/HO-1/GPX.

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