多种生物过程有助于转化增长因子β介导的癌症 耐药性
James P Heiserman1, Rosemary J Akhurst1,2,3
1Helen Diller Family Comprehensive Cancer Center, University of California San Francisco (UCSF), San Francisco, CA 94143, USA.
Cells
|October 15, 2025
概括
转化生长因子-β (TGF-β) 信号通过促进药物流量,DNA修复和免疫抑制来驱动癌症治疗耐药性. 准TGF-β通路对于克服治疗障碍和改善患者的治疗结果至关重要.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 治疗耐药性是癌症治疗的一个重大挑战.
- 转化生长因子-β (TGF-β) 信号与各种癌症的耐药性有关.
- 矛盾的是,癌症疗法可以增加TGF-β的释放,加剧耐药性.
研究的目的:
- 阐明TGF-β信号传导对抗癌症治疗的分子机制.
- 突出TGF-β在通过各种细胞和微环境变化中介抗性的作用.
- 强调需要进一步研究克服耐药性的TGF-β向策略.
主要方法:
- 对TGF-β信号传递在癌症治疗耐药性方面的现有文献的审查和综合.
- 分析分子机制,包括基因表达,蛋白质信号和细胞过程.
- 检查TGF-β对瘤微环境和免疫细胞的影响.
主要成果:
- TGF-β信号传递通过药物排放,增强DNA修复和细胞外基质重塑促进抗药性.
- 它激活了亲存活通路 (EGFR,Bcl-2,AKT-mTOR) 并驱动了上皮细胞到介质细胞的过渡,导致瘤异质性和干状状态.
- 在瘤微环境中,TGF-β通过激活癌症相关纤维细胞和抑制细胞毒性免疫细胞,同时促进调节细胞,促进免疫抑制.
结论:
- TGF-β信号传递是多面性癌症治疗耐药性的关键驱动因素.
- 了解这些机制对于开发新的治疗策略至关重要.
- 准TGF-β通路为组合疗法和克服耐药性提供了一个有希望的途径.
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