MAP激酶与前列腺癌。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2011-10-20 DOI:10.1155/2012/169170
Gonzalo Rodríguez-Berriguete, Benito Fraile, Pilar Martínez-Onsurbe, Gabriel Olmedilla, Ricardo Paniagua, Mar Royuela
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引用次数: 126

摘要

三种主要的丝裂原活化蛋白激酶(MAPKs) p38、JNK和ERK是广泛参与细胞功能的信号转导,包括存活、凋亡和细胞分化。虽然JNK和p38通常与细胞死亡和肿瘤抑制有关,但ERK在细胞存活和肿瘤促进中发挥着突出作用,以响应广泛的刺激,如细胞因子、生长因子、紫外线辐射、缺氧或药物化合物。然而,越来越多的证据支持JNK和p38也有助于许多恶性肿瘤的发展。在本文中,我们将重点关注MAPK通路在前列腺癌中的作用,包括鲜为人知的ERK5通路,通过其对细胞凋亡、存活、转移潜能和雄激素非依赖性生长的影响,作为促瘤或抗瘤介质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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MAP Kinases and Prostate Cancer.

The three major mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK are signal transducers involved in a broad range of cell functions including survival, apoptosis, and cell differentiation. Whereas JNK and p38 have been generally linked to cell death and tumor suppression, ERK plays a prominent role in cell survival and tumor promotion, in response to a broad range of stimuli such as cytokines, growth factors, ultraviolet radiation, hypoxia, or pharmacological compounds. However, there is a growing body of evidence supporting that JNK and p38 also contribute to the development of a number of malignances. In this paper we focus on the involvement of the MAPK pathways in prostate cancer, including the less-known ERK5 pathway, as pro- or antitumor mediators, through their effects on apoptosis, survival, metastatic potential, and androgen-independent growth.

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