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癌症转移和化学抵抗中的STAT3驱动的EMT:一篇综述
Yu Tian1, Min Tang2, Meng Qiao3
1Research Center, the Huizhou Central People's Hospital, Guangdong Medical University, Huizhou, Guangdong, China.
International journal of biological macromolecules
|March 13, 2026
概括
信号转换器和转录3激活器 (STAT3) 驱动上皮质-介质酶转换 (EMT),促进癌症转移和化疗耐药性. 针对STAT3-EMT途径提供了一个有希望的策略,以克服癌症治疗中的这些挑战.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 癌症的进展和化疗耐药性是临床的关键挑战.
- 表皮-介质细胞过渡 (EMT) 是推动这些问题的关键生物机制.
- 信号转换器和转录3激活器 (STAT3) 在癌症生物学中发挥着重要作用.
研究的目的:
- 审查STAT3在促进EMT方面的多方面的作用.
- 阐明STAT3介导的EMT如何促进癌症转移和化学抵抗.
- 讨论针对STAT3/EMT轴的潜在治疗策略.
主要方法:
- 文献综述侧重于癌症中的STAT3和EMT.
- 对将STAT3激活与EMT转录因子联系起来的分子机制的分析 (TWIST,SNAIL,ZEB1/2).
- 检查STAT3在瘤微环境 (TME) 和化学抵抗通路中的作用.
主要成果:
- 在人类癌症中,STAT3被上调,并通过调节关键转录因子来诱导EMT.
- EMT促进癌细胞的移动性,入侵和生存,导致转移.
- STAT3-EMT轴通过药物排放,抗亡蛋白和生存途径来增强化学抵抗.
- 在TME中,STAT3的激活会产生一种免疫抑制的环境.
结论:
- 用抑制剂,RNA干扰或天然化合物向STAT3介导的EMT显示了减少转移和化学抵抗的潜力.
- 开发精确的STAT3抑制剂和理解EMT动态仍然是一个挑战.
- 未来的研究应该探索组合疗法和先进技术,以制定有效的癌症治疗策略.
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