细胞可塑性和去分化:癌症干细胞、缺氧、细胞损伤和炎症之间的联系

A. Wijaya
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摘要

细胞可塑性是细胞分化程度的双向动态变化的概念,它涉及生物体生命周期内的再生、修复和组织更新。在ipcs的发现过程中,细胞的可塑性和去分化过程被很好地记录下来,通过将几种转录因子(称为Yamanaka因子)引入到终末分化的体细胞中,并恢复到多能状态,即ESCs。iPSCs能够表现出内皮干细胞分化的潜力,可以产生外胚层、中胚层和内胚层细胞谱系。在肿瘤生物学中,肿瘤的可塑性也有类似的调控作用,对维持肿瘤的完整性和生存,特别是对维持CSCs的数量起着重要作用。对细胞可塑性调节的各种研究表明,多种因素参与其中,例如缺氧、细胞损伤和炎症。细胞对缺氧、细胞损伤和炎症的反应是通过化学引诱剂来吸引修复细胞回到受伤部位。干细胞的归巢机制涉及EMT促进干细胞向损伤部位迁移,从而导致组织再生。另一方面,肿瘤转移也与EMT过程有关。EMT显示细胞特性的改变与去分化和缺氧反应有关。缺氧条件可以保存正常干细胞和CSCs的干细胞性。HIF通过与HRE结合与DNA相互作用,在缺氧条件下防止降解。HRE的激活可触发多种信号蛋白的转录,这些信号蛋白参与细胞的生长、增殖和存活。因此,我们认为细胞损伤、缺氧和炎症可程序化细胞进行去分化过程,并参与EMT调控。存在于异质肿瘤细胞群中的CSCs与正常干细胞一样,通过去分化在安静和活跃状态下进行动态调节。了解CSCs如何调节其活跃和安静状态的动态,可以为新型CSCs靶向治疗的开发提供重要信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cellullar Plasticity and Dedifferentiation: A Link Between Cancer Stem Cells, Hypoxia, Cell Injury, and Inflammation
Cellular plasticity is the concept of bidirectional dynamics change cells differentiation degree which involved in the regeneration, repair and tissue turnover along the organism livespan. Cellular plasticity and dedifferentiation process are well documented in the discovery of iPCSs by introducing several transcriptional factors known as Yamanaka factor to terminally differentiated somatic cells and reverted into pluripotent state as the ESCs. iPSCs are able to exhibit ESCs differentiation potential which could produce ectodermic, mesodermic, and endodermic cell lineage. In tumour biology, the tumour plasticity also have a similar regulation and play an imporant role for maintaining tumour integrity and survival, particularly in maintaining CSCs population. Various study of cellular plasticity regulation has shown that various factors are involved, in example hypoxia, cell injury, and inflammation. Cells respond to hypoxia, cell injury, and inflammation by chemoattractant which attract repair cells to homing towards injured sites. The homing mechanism of stem cells involved EMT to facilitates migration of stem cells towards injured sites, thus leading to tissue regeneration. On the other hand, cancer metastasis also showed a connection with EMT process. EMT which showed a change in cell properties are linked to dedifferentiation and hypoxia response. Hypoxia condition has been known to preserve and both normal stem cells and CSCs stemness. HIF which protected from degradation in hypoxia condition interact with DNA by binding to HRE. HRE activation trigger transcription of numerous signalling protein which involved in stemness, cell proliferation and survival. Therefore it is concluded that cell injury, hypoxia, and inflammation could programmed cells to undergo dedifferentiation process and involved in EMT regulations. CSCs which resides insides heterogeneous tumour cells population are though to be dynamicly regulate itself in the quietscent and active state through dedifferentiation like the normal stem cells. Understanding how CSCs regulates its active an quietscent state dynamics could provide an important information for novel CSCs targeted therapy development. 
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