Journal of gastrointestinal oncology · 2026
Establishment of a chemoradio-resistance colorectal cancer cell model and its changes in biological behavior.
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Liu Shan, Zhang Zeng, An Qian, Jia Yue, Su Qin, Zhu Dezhi, Luan Likun, Yang Hongying, Chuan Zhirui, Liu Xinyuan, Wang Siyu, Liu Yanyan, Fu Fenglian, Sun Qiong, Ma Luyao, Yang Juanrong, Zhang Yiming, Duan Mingzhi, Yao Peijun, Yang Changqing, Xing Yiming, Shen Hongmei, Jiang Yongxin
Аннотация
BACKGROUND: Colorectal cancer (CRC) is the most prevalent and malignant gastrointestinal tract tumor. The incidence remains high, and the issue of resistance to radiotherapy and chemotherapy is prominent. The aims were therefore to establish a model for radio- and chemoresistance in CRC, elucidating the underlying mechanism that could help identify measures to reverse its resistance and improve the clinical efficacy of radiotherapy and chemotherapy.
METHODS: A HCT116 and HT29 cell model of radiotherapy and chemotherapy resistance in CRC was established by simulating clinical high-dose shock therapy as a key in vitro method. For the in vivo animal studies, healthy 6-week-old BALB/c nude mice (both genders) were used. The changes in its biological behavior were studied to provide a theoretical basis for improving the efficacy of radiotherapy and chemotherapy in clinical practice.
RESULTS: We successfully established a CRC cell line with radio- and chemoresistance, and it exhibited stronger potential for cell proliferation, colony formation, invasion, and migration than its parental cell line. Furthermore, in nude mouse models, the resistant cells showed stronger tumorigenicity and stronger liver and lung metastasis ability than the parental cells.
CONCLUSIONS: This research helps elucidate the molecular mechanism of chemo- and radiotherapy resistance in CRC and can potentially improve the molecular diagnosis and gene therapy of CRC.
METHODS: A HCT116 and HT29 cell model of radiotherapy and chemotherapy resistance in CRC was established by simulating clinical high-dose shock therapy as a key in vitro method. For the in vivo animal studies, healthy 6-week-old BALB/c nude mice (both genders) were used. The changes in its biological behavior were studied to provide a theoretical basis for improving the efficacy of radiotherapy and chemotherapy in clinical practice.
RESULTS: We successfully established a CRC cell line with radio- and chemoresistance, and it exhibited stronger potential for cell proliferation, colony formation, invasion, and migration than its parental cell line. Furthermore, in nude mouse models, the resistant cells showed stronger tumorigenicity and stronger liver and lung metastasis ability than the parental cells.
CONCLUSIONS: This research helps elucidate the molecular mechanism of chemo- and radiotherapy resistance in CRC and can potentially improve the molecular diagnosis and gene therapy of CRC.