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ERK/MAPK信号通路与肿瘤发生

ERK/MAPK signalling pathway and tumorigenesis.

作者信息

Guo Yan-Jun, Pan Wei-Wei, Liu Sheng-Bing, Shen Zhong-Fei, Xu Ying, Hu Ling-Ling

机构信息

Department of Human Anatomy and Embryology, College of Medicine, Jiaxing University, Jiaxing, Zhejiang 314000, P.R. China.

出版信息

Exp Ther Med. 2020 Mar;19(3):1997-2007. doi: 10.3892/etm.2020.8454. Epub 2020 Jan 15.

DOI:10.3892/etm.2020.8454
PMID:32104259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7027163/
Abstract

Mitogen-activated protein kinase (MAPK) cascades are key signalling pathways that regulate a wide variety of cellular processes, including proliferation, differentiation, apoptosis and stress responses. The MAPK pathway includes three main kinases, MAPK kinase kinase, MAPK kinase and MAPK, which activate and phosphorylate downstream proteins. The extracellular signal-regulated kinases ERK1 and ERK2 are evolutionarily conserved, ubiquitous serine-threonine kinases that regulate cellular signalling under both normal and pathological conditions. ERK expression is critical for development and their hyperactivation plays a major role in cancer development and progression. The Ras/Raf/MAPK (MEK)/ERK pathway is the most important signalling cascade among all MAPK signal transduction pathways, and plays a crucial role in the survival and development of tumour cells. The present review discusses recent studies on Ras and ERK pathway members. With respect to processes downstream of ERK activation, the role of ERK in tumour proliferation, invasion and metastasis is highlighted, and the role of the ERK/MAPK signalling pathway in tumour extracellular matrix degradation and tumour angiogenesis is emphasised.

摘要

丝裂原活化蛋白激酶(MAPK)级联反应是关键的信号通路,可调节多种细胞过程,包括增殖、分化、凋亡和应激反应。MAPK通路包括三种主要激酶,即MAPK激酶激酶、MAPK激酶和MAPK,它们激活并磷酸化下游蛋白。细胞外信号调节激酶ERK1和ERK2在进化上保守,是普遍存在的丝氨酸 - 苏氨酸激酶,在正常和病理条件下均调节细胞信号传导。ERK表达对发育至关重要,其过度激活在癌症发展和进展中起主要作用。Ras/Raf/MAPK(MEK)/ERK通路是所有MAPK信号转导通路中最重要的信号级联反应,在肿瘤细胞的存活和发展中起关键作用。本综述讨论了关于Ras和ERK通路成员的最新研究。关于ERK激活下游的过程,强调了ERK在肿瘤增殖、侵袭和转移中的作用,并着重阐述了ERK/MAPK信号通路在肿瘤细胞外基质降解和肿瘤血管生成中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/06455966afd0/etm-19-03-1997-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/beba3c3450fb/etm-19-03-1997-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/bd1519c84fe9/etm-19-03-1997-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/0ce2683ecd2d/etm-19-03-1997-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/4899ec0172f1/etm-19-03-1997-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/06455966afd0/etm-19-03-1997-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/beba3c3450fb/etm-19-03-1997-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/bd1519c84fe9/etm-19-03-1997-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/0ce2683ecd2d/etm-19-03-1997-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/4899ec0172f1/etm-19-03-1997-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dc4/7027163/06455966afd0/etm-19-03-1997-g04.jpg

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