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表皮质-介质细胞可塑性的动力驱动癌症耐药性
Rashmi Bangarh1, Reena V Saini1, Adesh K Saini1
1Department of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, India.
表皮-介质细胞过渡 (EMT) 驱动癌症的进展和治疗抵抗. 针对EMT途径提供了一个有希望的策略,以克服各种癌症中免疫疗法和化疗的耐药性.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 分子生物学分子生物学
背景情况:
- 表皮-介质细胞过渡 (EMT) 是一个细胞过程,对胚胎发育和伤口愈合至关重要.
- EMT与癌症的进展有关,增加瘤细胞的运动性并导致转移.
- 此外,EMT还能对癌症疗法产生抗性,包括免疫疗法和化疗.
研究的目的:
- 审查管理EMT及其相反的分子机制,介质细胞-上皮细胞过渡 (MET).
- 讨论EMT对瘤微环境和癌症治疗耐药性的影响.
- 探索针对EMT作为克服治疗耐药性的战略.
主要方法:
- 关于EMT,MET和癌症治疗耐药性的研究的文献综述.
- 分析涉及EMT的分子机制,信号网络和细胞状态.
- 对EMT在免疫疗法和化疗耐药性中的作用的研究结果的综合.
主要成果:
- EMT增强了瘤细胞的运动性,破坏了细胞-细胞粘附,并促进了入侵.
- EMT是由转录因子,翻译后修改,细胞因子信号传递和microRNAs控制的.
- EMT对免疫疗法和化疗的耐药性有显著的贡献.
- MET,反向过程,与瘤转移抑制有关.
结论:
- 在癌症进展和治疗耐药性方面,EMT是关键因素.
- 了解EMT的分子复杂性是开发有效癌症治疗的关键.
- 针对EMT是一个可行的策略,通过克服治疗耐药性来改善患者的治疗结果.
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