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Background <p>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.</p> Methods <p>A nude mouse xenograft model using human colorectal cancer HCT116 and HCT116-chemo-radiation resistant (HCT116-CRR) cells was established.</p> Results <p>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.</p> Conclusions <p>These findings provide both mechanistic insights and experimental validation for the potential application of ARE as a radiosensitizer in colorectal cancer radiotherapy.</p>

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Artemether as a modulator of EMT in colorectal cancer: enhancing radiosensitivity and reversing chemo-radiation resistance

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月4日

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  • Lv Ge,
  • Shan Liu,
  • Shenglan Yu,
  • Ming Li,
  • Wanni Zhang,
  • Chunmao Xie,
  • Zhuo Gao,
  • Sijia Tang,
  • Minqi Xiao,
  • Tao Zou,
  • Yongxin Jiang,
  • Hu Lu

摘要

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.