MAP Kinases and Prostate Cancer.
MAP Kinases and Prostate Cancer.
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DOI：
10.1155/2012/169170
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Royuela M
中科院分区：
文献类型：
--
作者：
Rodríguez-Berriguete G;Fraile B;Martínez-Onsurbe P;Olmedilla G;Paniagua R;Royuela M
三种主要的促分裂原活化蛋白激酶（MAPK）p38、JNK和ERK是参与广泛的细胞功能（包括存活、凋亡和细胞分化）的信号转导子。JNK和p38通常与细胞死亡和肿瘤抑制有关，而ERK在细胞存活和肿瘤促进中起着重要作用，响应于广泛的刺激，如细胞因子、生长因子、紫外线辐射、缺氧或药理学化合物。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，我们专注于参与的MAPK途径在前列腺癌，包括鲜为人知的ERK 5途径，作为亲或抗肿瘤介质，通过其对细胞凋亡，生存，转移潜力，和雄激素非依赖性生长的影响。
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.