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YAP在程序性细胞死亡中的生物学特性。

The biology of YAP in programmed cell death.

作者信息

Cheng Yifan, Mao Misha, Lu Yong

机构信息

Department of Gastrointestinal Surgery, Taizhou Hospital of Zhejiang Province, Wenzhou Medical University, Taizhou, Zhejiang, China.

Department of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, Zhejiang, China.

出版信息

Biomark Res. 2022 May 23;10(1):34. doi: 10.1186/s40364-022-00365-5.

Abstract

In the last few decades, YAP has been shown to be critical in regulating tumor progression. YAP activity can be regulated by many kinase cascade pathways and proteins through phosphorylation and promotion of cytoplasmic localization. Other factors can also affect YAP activity by modulating its binding to different transcription factors (TFs). Programmed cell death (PCD) is a genetically controlled suicide process present with the scope of eliminating cells unnecessary or detrimental for the proper development of the organism. In some specific states, PCD is activated and facilitates the selective elimination of certain types of tumor cells. As a candidate oncogene correlates with many regulatory factors, YAP can inhibit or induce different forms of PCD, including apoptosis, autophagy, ferroptosis and pyroptosis. Furthermore, YAP may act as a bridge between different forms of PCD, eventually leading to different outcomes regarding tumor development. Researches on YAP and PCD may benefit the future development of novel treatment strategies for some diseases. Therefore, in this review, we provide a general overview of the cellular functions of YAP and the relationship between YAP and PCD.

摘要

在过去几十年中,YAP已被证明在调节肿瘤进展中起关键作用。YAP的活性可通过许多激酶级联途径和蛋白质通过磷酸化以及促进细胞质定位来调节。其他因素也可通过调节YAP与不同转录因子(TFs)的结合来影响YAP的活性。程序性细胞死亡(PCD)是一种受基因控制的自杀过程,其作用是消除对生物体正常发育不必要或有害的细胞。在某些特定状态下,PCD被激活并促进某些类型肿瘤细胞的选择性清除。作为一种与许多调节因子相关的候选癌基因,YAP可抑制或诱导不同形式的PCD,包括细胞凋亡、自噬、铁死亡和焦亡。此外,YAP可能在不同形式的PCD之间起桥梁作用,最终导致肿瘤发展的不同结果。对YAP和PCD的研究可能有利于某些疾病新型治疗策略的未来发展。因此,在本综述中,我们概述了YAP的细胞功能以及YAP与PCD之间的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f784/9128211/72ac2253f445/40364_2022_365_Fig1_HTML.jpg

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