非典型MAP激酶信号通路ERK3/4-MK5对肿瘤的促进和抑制作用。

Q2 Biochemistry, Genetics and Molecular Biology
Sergiy Kostenko, Gianina Dumitriu, Ugo Moens
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引用次数: 39

摘要

信号转导途径的扰动作用,包括丝裂原活化蛋白(MAP)激酶途径,是许多癌症的特征之一。虽然典型的MAP激酶途径ERK1/2-MEK1/2、p38MAPK和JNK的含义已经得到很好的证实,但最近的研究结果表明,非典型MAP激酶ERK3/4-MK5也可能参与肿瘤发生过程。值得注意的是,ERK3/4-MK5通路在细胞培养和免疫模型中似乎具有抗癌和促癌特性。本文综述了在不同癌症中检测到的编码ERK3、ERK4和MK5的基因突变,报道了这些蛋白质在人类肿瘤中的异常表达水平,并讨论了该途径诱导衰老、刺激血管生成和侵袭性的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Tumour promoting and suppressing roles of the atypical MAP kinase signalling pathway ERK3/4-MK5.

Tumour promoting and suppressing roles of the atypical MAP kinase signalling pathway ERK3/4-MK5.

Tumour promoting and suppressing roles of the atypical MAP kinase signalling pathway ERK3/4-MK5.

Tumour promoting and suppressing roles of the atypical MAP kinase signalling pathway ERK3/4-MK5.

Perturbed action of signal transduction pathways, including the mitogen-activated protein (MAP) kinase pathways, is one of the hallmarks of many cancers. While the implication of the typical MAP kinase pathways ERK1/2-MEK1/2, p38MAPK and JNK is well established, recent findings illustrate that the atypical MAP kinase ERK3/4-MK5 may also be involved in tumorigenic processes. Remarkably, the ERK3/4-MK5 pathway seems to possess anti-oncogenic as well as pro-oncogenic properties in cell culture and aninal models. This review summarizes the mutations in the genes encoding ERK3, ERK4 and MK5 that have been detected in different cancers, reports aberrant expression levels of these proteins in human tumours, and discusses the mechanisms by which this pathway can induce senescence, stimulate angiogenesis and invasiveness.

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来源期刊
Journal of Molecular Signaling
Journal of Molecular Signaling Biochemistry, Genetics and Molecular Biology-Biochemistry
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期刊介绍: Journal of Molecular Signaling is an open access, peer-reviewed online journal that encompasses all aspects of molecular signaling. Molecular signaling is an exponentially growing field that encompasses different molecular aspects of cell signaling underlying normal and pathological conditions. Specifically, the research area of the journal is on the normal or aberrant molecular mechanisms involving receptors, G-proteins, kinases, phosphatases, and transcription factors in regulating cell proliferation, differentiation, apoptosis, and oncogenesis in mammalian cells. This area also covers the genetic and epigenetic changes that modulate the signaling properties of cells and the resultant physiological conditions.
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