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

BackgroundColorectal 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 resultsIn 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.ConclusionIn 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.