Demonstrates that artemether improves radiosensitivity in colorectal cancer, suggesting new treatment approaches.
Background The efficacy of conventional chemoradiotherapy for colorectal cancer is often limited by resistance, with epithelial-mesenchymal transition being a key mechanism. Although the artemisinin derivative artemether (ARE) has shown antitumor potential, it remains unclear whether it can enhance radiosensitivity and reverse chemo-radiation resistance in colorectal cancer by regulating EMT. This study aimed to investigate the radiosensitizing and resistance-reversing effects of ARE on human colorectal cancer xenografts in nude mice and to elucidate the underlying mechanism related to EMT regulation. Methods A nude mouse xenograft model using human colorectal cancer HCT116 and HCT116-chemo-radiation resistant (HCT116-CRR) cells was established. Results ARE combined with radiotherapy suppressed tumor growth in nude mice and induced cell death via necrosis and apoptosis. After ARE combined with radiotherapy, β-Catenin was increased in human colorectal cancer HCT116 cells implanted in nude mice, while Vimentin was decreased. In HCT116-CRR cells transplanted into nude mice, the E-cadherin and β-Catenin were upregulated, whereas N-Cadherin, Vimentin, Snail, Slug, and Twist were downregulated. ARE effectively significantly enhanced radiosensitivity and reversed chemo-radiation resistance by suppressing EMT. Conclusions These findings provide both mechanistic insights and experimental validation for the potential application of ARE as a radiosensitizer in colorectal cancer radiotherapy.
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