揭开表皮质可塑性的复杂性:从主调节器转录因子到非编码RNA
Charlene Waryah1,2, Eric Alves1,2, Roberta Mazzieri3,4
1Cancer Epigenetics Group, Harry Perkins Institute of Medical Research, Perth, WA 6009, Australia.
Cancers
|June 28, 2023
概括
癌细胞通过细胞可塑性进行适应,这一过程与上皮-介质细胞过渡 (EMT) 有关. 这篇评论探讨了EMT.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 细胞可塑性 细胞可塑性
背景情况:
- 癌细胞表现出细胞可塑性,使其能够适应瘤微环境.
- 这种可塑性会影响瘤茎,转移,耐药性和免疫逃避.
- 表皮质可塑性,特别是表皮质-介质细胞过渡 (EMT) 是一个关键机制.
研究的目的:
- 审查调节癌症上皮质可塑性的因素的复杂相互作用.
- 探索表皮层-介质细胞转换 (EMT) 现型的频谱.
- 根据这些机制,确定潜在的治疗目标和途径.
主要方法:
- 关于癌症中的细胞可塑性和上皮-介质细胞转变 (EMT) 的文献综述.
- 对转录因子,表观遗传修饰剂和非编码RNA之间的交叉对话进行分析.
- 检查EMT的代谢,转录和表观遗传调节.
主要成果:
- 表皮-介质细胞过渡 (EMT) 是一个频谱,而不是一个二进制状态,涉及准表皮和准介质细胞表型.
- 细胞代谢,转录组调节和表观遗传机制复杂地控制表皮质可塑性.
- 转录因子,表观遗传修饰剂和非编码RNA之间的相互作用至关重要.
结论:
- 了解上皮质可塑性和EMT的多面性质对于癌症治疗至关重要.
- 针对复杂的监管网络提供了有希望的治疗策略.
- 在EMT过渡期间操纵癌症免疫性可以提高治疗效率.
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