肺瘤微环境中的相互作用和通信:化疗/放射治疗耐药性机制和治疗点
Yuan Feng1, Ying Jiang2, Lin Yang1
1Guangxi University of Chinese Medicine, Nanning, China.
Journal of drug targeting
|January 16, 2025
概括
肺瘤微环境 (TME) 促进癌症对治疗的抵抗力. 针对TME组件,如免疫细胞和细胞外基质 (ECM),可以克服这种阻力.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 免疫学 免疫学 免疫学
背景情况:
- 肺瘤微环境 (TME) 包括癌细胞,层细胞,免疫细胞和细胞外基质 (ECM).
- 这种复杂的环境创造了一个硬,缺氧,酸性和免疫抑制的环境,促进瘤抵抗细胞死亡,入侵和转移.
- 通过激活抗亡途径 (PI3K/Akt,STAT3,NF-κB) 和促进免疫逃逸,TME有助于化疗/放射治疗耐药性.
研究的目的:
- 审查肺TME内部复杂的相互作用.
- 阐明缺氧,免疫逃避和ECM重塑在肺癌耐药性中的作用.
- 讨论针对肺TME的当前和新兴治疗策略,以克服治疗耐药性.
主要方法:
- 临床前和临床研究的文献综述.
- 对推动TME介导抗性的分子机制的分析.
- 综合了针对TME组件的治疗干预的数据.
主要成果:
- 肺部TME通过各种细胞和分子机制积极促进对化疗和放射治疗的耐药性.
- 缺氧,免疫抑制和ECM重塑是导致治疗失败的关键因素.
- 肺部瘤细胞使用多药性耐药性和抗氧化剂系统来生存治疗.
结论:
- 了解肺TME动态对于开发有效的癌症疗法至关重要.
- 针对特定的TME组件,包括免疫检查点 (例如PD-1) 和生长因子 (例如IGF-2),在克服抵抗方面显示出希望.
- 调节TME的联合治疗策略对于改善肺癌患者的治疗结果至关重要.
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