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首页|期刊导航|天津师范大学学报(自然科学版)|利多卡因对结肠癌细胞增殖和迁移的作用及其机制

利多卡因对结肠癌细胞增殖和迁移的作用及其机制

罗曼 宋振国

天津师范大学学报(自然科学版)2025,Vol.45Issue(1):22-26,5.
天津师范大学学报(自然科学版)2025,Vol.45Issue(1):22-26,5.DOI:10.19638/j.issn1671-1114.20250104

利多卡因对结肠癌细胞增殖和迁移的作用及其机制

Effects and mechanisms of lidocaine on proliferation and migration of colorectal cancer cells

罗曼 1宋振国2

作者信息

  • 1. 天津医科大学肿瘤医院麻醉科,天津 300060||天津医科大学肿瘤医院国家肿瘤临床医学研究中心,天津 300060||天津医科大学肿瘤医院天津市恶性肿瘤临床医学研究中心||天津医科大学肿瘤医院天津市"肿瘤防治"重点实验室,天津 300060||天津市第五中心医院麻醉科,天津 300450
  • 2. 天津医科大学肿瘤医院麻醉科,天津 300060||天津医科大学肿瘤医院国家肿瘤临床医学研究中心,天津 300060||天津医科大学肿瘤医院天津市恶性肿瘤临床医学研究中心||天津医科大学肿瘤医院天津市"肿瘤防治"重点实验室,天津 300060
  • 折叠

摘要

Abstract

To investigate the therapeutic effects and mechanism of lidocaine on colorectal cancer,the human colorectal cancer cell line LOVO and HCT116 were selected for grouped experiments.LOVO and HCT116 cells were treated with 0 mmol/L and 2 mmol/L concentrations of lidocaine for 24 h.The cell growth was evaluated using CCK-8 and clonogenic assays,while cell motility was assessed through Transwell and wound healing assays.Ferroptosis was measured using immunoblotting and iron detection kits,and the activation of PI3K/Akt/mTOR signaling pathway was evaluated by immunoblotting.The results showed that:① Lidocaine significantly inhibited the growth and motility of human colorectal cancer cells compared with control group;② Lidocaine promoted ferroptosis in colorectal cancer cells;③ The antitumor effects of lidocaine were associated with the inhibition of PI3K/Akt/mTOR signaling pathway,which is crucial for cell survival and growth.Overall,lidocaine exerts antitu-mor effects on colorectal cancer cells by inhibiting cell growth and motility,promoting ferroptosis,and suppressing the PI3K/Akt/mTOR signaling pathway.

关键词

结肠癌/利多卡因/细胞生长/铁死亡/PI3K/Akt/mTOR信号通路

Key words

colorectal cancer/lidocaine/cell growth/ferroptosis/PI3K/Akt/mTOR signaling pathway

分类

临床医学

引用本文复制引用

罗曼,宋振国..利多卡因对结肠癌细胞增殖和迁移的作用及其机制[J].天津师范大学学报(自然科学版),2025,45(1):22-26,5.

基金项目

天津市医学重点学科(专科)建设项目(TJYXZDXK-009A). (专科)

天津师范大学学报(自然科学版)

OA北大核心

1671-1114

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