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丝裂原活化蛋白激酶激酶激酶4(MAP3K4)在癌症中的激酶作用及双重角色

MAP3K4 kinase action and dual role in cancer.

作者信息

Huang Yuxin, Wang Guanwen, Zhang Ningning, Zeng Xiaohua

机构信息

Department of Breast Cancer Center, Chongqing University Cancer Hospital, School of Medicine, Chongqing University, Chongqing, China.

Department of Breast Cancer Center, Chongqing University Cancer Hospital, Chongqing, China.

出版信息

Discov Oncol. 2024 Apr 3;15(1):99. doi: 10.1007/s12672-024-00961-x.

DOI:10.1007/s12672-024-00961-x
PMID:38568424
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10992237/
Abstract

It is commonly known that the MAPK pathway is involved in translating environmental inputs, regulating downstream reactions, and maintaining the intrinsic dynamic balance. Numerous essential elements and regulatory processes are included in this pathway, which are essential to its functionality. Among these, MAP3K4, a member of the serine/threonine kinases family, plays vital roles throughout the organism's life cycle, including the regulation of apoptosis and autophagy. Moreover, MAP3K4 can interact with key partners like GADD45, which affects organism's growth and development. Notably, MAP3K4 functions as both a tumor promotor and suppressor, being activated by a variety of factors and triggering diverse downstream pathways that differently influence cancer progression. The aim of this study is to provide a brief overview of physiological functions of MAP3K4 and shed light on its contradictory roles in tumorigenesis.

摘要

众所周知,丝裂原活化蛋白激酶(MAPK)信号通路参与转导环境信号输入、调节下游反应并维持内在动态平衡。该信号通路包含众多关键元件和调控过程,这些对其功能至关重要。其中,丝氨酸/苏氨酸激酶家族成员丝裂原活化蛋白激酶激酶激酶4(MAP3K4)在生物体的整个生命周期中发挥着至关重要的作用,包括对细胞凋亡和自噬的调控。此外,MAP3K4可与生长停滞和DNA损伤诱导蛋白45(GADD45)等关键伙伴相互作用,从而影响生物体的生长发育。值得注意的是,MAP3K4既作为肿瘤促进因子又作为肿瘤抑制因子发挥作用,它被多种因素激活并触发不同的下游信号通路,这些通路对癌症进展产生不同的影响。本研究的目的是简要概述MAP3K4的生理功能,并阐明其在肿瘤发生中的矛盾作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/635993d00599/12672_2024_961_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/f9d99f90bb77/12672_2024_961_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/1a19ee80e8cd/12672_2024_961_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/3b70a59a24e5/12672_2024_961_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/635993d00599/12672_2024_961_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/f9d99f90bb77/12672_2024_961_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/1a19ee80e8cd/12672_2024_961_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/3b70a59a24e5/12672_2024_961_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/10992237/635993d00599/12672_2024_961_Fig4_HTML.jpg

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