激活的CD36-Src轴在高脂肪环境中促进肺腺癌细胞的增殖和参与actin重塑的转移
Li-Zhong Liu1, Bowen Wang1,2, Rui Zhang3
1Department of Physiology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Cell death & disease
|August 23, 2023
概括
高脂肪饮食通过脂肪酸转位酶CD36.6促进肺腺癌 (LUAD) 的生长和转移. 向CD36为肥胖患者的LUAD提供了潜在的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 代谢过程中的代谢.
背景情况:
- 肥胖和脂质代谢障碍正在增加肺癌风险因素.
- 脂肪酸转位酶CD36调解细胞脂肪酸的吸收.
- 在高脂肪条件下,CD36在肺腺癌 (LUAD) 进展中的作用尚不清楚.
研究的目的:
- 研究CD36在高脂肪环境中促进LUAD生长和转移的机制.
- 探索CD36作为LUAD的潜在治疗点.
主要方法:
- 在体外研究中,使用用棕酸 (PA) 或高脂肪饮食 (HFD) 治疗的LUAD细胞系.
- 在活体研究中,使用HFD下的异种移植的LUAD细胞的小鼠模型进行了实验.
- 分析包括Src,Akt,ERK和Rac1在内的信号通路.
- 评估雅丁重塑和细胞转移的情况.
主要成果:
- PA和HFD促进了依赖CD36.6的LUAD细胞增殖和转移.
- 在PA刺激后,CD36转移到细胞膜,与Src酶相互作用.
- 激活Src,Akt和ERK通路,可以促使扩散和转移.
- CD36促进了乙重塑和细胞表面突起,增强了转移.
- 在体内,HFD增加了瘤生长和转移,CD36敲击阻断了这种转移.
- 抑制CD36显著降低了LUAD转移.
结论:
- CD36启动Src信号,在高脂肪环境中促进LUAD细胞的增殖和转移.
- 在LUAD细胞转移中,CD36介导的活性蛋白重塑至关重要.
- CD36代表了LUAD的一个有前途的治疗标,特别是在肥胖和代谢障碍的背景下.
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