Establishment of a chemoradio-resistance colorectal cancer cell model and its changes in biological behavior.

IF 2.1 4区 医学 Q3 GASTROENTEROLOGY & HEPATOLOGY
Journal of gastrointestinal oncology Pub Date : 2026-08-31 Epub Date: 2026-06-24 DOI:10.21037/jgo-2025-812
Shan Liu, Zeng Zhang, Qian An, Yue Jia, Qin Su, Dezhi Zhu, Likun Luan, Hongying Yang, Zhirui Chuan, Xinyuan Liu, Siyu Wang, Yanyan Liu, Fenglian Fu, Qiong Sun, Luyao Ma, Juanrong Yang, Yiming Zhang, Mingzhi Duan, Peijun Yao, Changqing Yang, Yiming Xing, Hongmei Shen, Yongxin Jiang
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引用次数: 0

Abstract

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.

结直肠癌放化疗耐药细胞模型的建立及其生物学行为的变化。
背景:结直肠癌(Colorectal cancer, CRC)是最常见的胃肠道恶性肿瘤。发病率居高不下,放疗和化疗耐药问题突出。因此,我们的目的是建立CRC的放射和化疗耐药模型,阐明其潜在机制,从而帮助确定逆转其耐药的措施,提高放疗和化疗的临床疗效。方法:以模拟临床大剂量休克治疗为关键体外方法,建立结直肠癌放化疗耐药HCT116和HT29细胞模型。在体内动物研究中,使用健康的6周龄BALB/c裸鼠(两性)。研究其生物学行为的变化,为临床提高放化疗疗效提供理论依据。结果:我们成功建立了一个具有放射和化学耐药的结直肠癌细胞系,它比亲本细胞系表现出更强的细胞增殖、集落形成、侵袭和迁移潜力。此外,在裸鼠模型中,耐药细胞比亲本细胞表现出更强的致瘤性和更强的肝、肺转移能力。结论:本研究有助于阐明结直肠癌化疗和放疗耐药的分子机制,有望提高结直肠癌的分子诊断和基因治疗水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.20
自引率
0.00%
发文量
171
期刊介绍: ournal of Gastrointestinal Oncology (Print ISSN 2078-6891; Online ISSN 2219-679X; J Gastrointest Oncol; JGO), the official journal of Society for Gastrointestinal Oncology (SGO), is an open-access, international peer-reviewed journal. It is published quarterly (Sep. 2010- Dec. 2013), bimonthly (Feb. 2014 -) and openly distributed worldwide. JGO publishes manuscripts that focus on updated and practical information about diagnosis, prevention and clinical investigations of gastrointestinal cancer treatment. Specific areas of interest include, but not limited to, multimodality therapy, markers, imaging and tumor biology.
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