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过氧化物还原酶家族在癌症信号传导中的作用。

The Role of Peroxiredoxin Family in Cancer Signaling.

作者信息

Kim Yosup, Jang Ho Hee

机构信息

Department of Health Sciences and Technology, Graduate School of Medicine, Gachon University, Incheon, Korea.

Department of Biochemistry, College of Medicine, Gachon University, Incheon, Korea.

出版信息

J Cancer Prev. 2019 Jun;24(2):65-71. doi: 10.15430/JCP.2019.24.2.65. Epub 2019 Jun 30.

Abstract

Peroxiredoxins (Prxs) are antioxidant enzymes that protect cells from oxidative stress by reducing intracellular accumulation of reactive oxygen species (ROS). In mammalian cells, the six Prx isoforms are ubiquitously expressed in diverse intracellular locations. They are involved in the regulation of various physiological processes including cell growth, differentiation, apoptosis, immune response and metabolism as well as intracellular ROS homeostasis. Although there are increasing evidences that Prxs are involved in carcinogenesis of many cancers, their role in cancer is controversial. The ROS levels in cancer cells are increased compared to normal cells, thus promoting cancer development. Nevertheless, for various cancer types, an overexpression of Prxs has been found to be associated with poor patient prognosis, and an increasing number of studies have reported that tumorigenesis is either facilitated or inhibited by regulation of cancer-associated signaling pathways. This review summarizes Prx isoforms and their basic functions, the relationship between the expression level and the physiological role of Prxs in cancer cells, and their roles in regulating cancer-associated signaling pathways.

摘要

过氧化物酶(Prxs)是一类抗氧化酶,通过减少细胞内活性氧(ROS)的积累来保护细胞免受氧化应激。在哺乳动物细胞中,六种Prx亚型在不同的细胞内位置普遍表达。它们参与多种生理过程的调节,包括细胞生长、分化、凋亡、免疫反应和代谢以及细胞内ROS稳态。尽管越来越多的证据表明Prxs参与了许多癌症的发生,但它们在癌症中的作用仍存在争议。与正常细胞相比,癌细胞中的ROS水平升高,从而促进癌症发展。然而,对于各种癌症类型,已发现Prxs的过表达与患者预后不良相关,并且越来越多的研究报告称,肿瘤发生可通过调节癌症相关信号通路而得到促进或抑制。本综述总结了Prx亚型及其基本功能、Prxs在癌细胞中的表达水平与生理作用之间的关系,以及它们在调节癌症相关信号通路中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c42/6619859/cfd65edad300/jcp-24-065f1.jpg

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