癌细胞可塑性,干细胞因子和治疗耐药性:它们是如何联系在一起的?
Homa Fatma1, Hifzur R Siddique2
1Molecular Cancer Genetics & Translational Research Lab, Section of Genetics, Department of Zoology, Aligarh Muslim University, Aligarh, UP, 202002, India.
Cancer metastasis reviews
|October 5, 2023
概括
癌细胞的可塑性,由表皮-介质细胞过渡 (EMT) 和干细胞因素驱动,促进瘤生长和耐药性. 针对这些机制为有效的癌症治疗和改善患者存活率提供了一个有希望的策略.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 癌症研究 癌症研究
背景情况:
- 细胞可塑性是发育过程中的自然适应机制.
- 异常的细胞可塑性是癌症的标志,有助于瘤的进展.
- 癌症干细胞 (CSCs) 是这种可塑性的关键驱动力.
研究的目的:
- 审查细胞可塑性,EMT和干细胞因子在癌症中的多方面的作用.
- 阐明它们在瘤发作,进展,重编程和治疗耐药性的参与.
- 探索针对这一轴的治疗策略,以改善癌症管理.
主要方法:
- 文献综述侧重于细胞可塑性,EMT,干细胞因子 (OCT4,NANOG,SOX2) 和信号通路.
- 对这些因素在驱动癌症表型中的相互作用进行分析.
- 讨论潜在的治疗干预措施.
主要成果:
- 癌细胞可塑性,EMT和干细胞因素促进CSC表型的维持.
- 这些因素有助于增加细胞迁移,瘤异质性和药物耐受性.
- 这种复杂的关系促进了免疫逃避和获得的耐药性.
结论:
- 针对细胞可塑性,EMT,表观遗传可塑性和干细胞因素的干预措施对于有效的癌症治疗至关重要.
- 调节这个轴可以克服治疗耐药性并改善患者的治疗结果.
- 本次审查强调了向癌细胞可塑性和CSCs的治疗潜力.
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