Phosphorylation of myofibrillogenesis regulator-1 activates the MAPK signaling pathway and induces proliferation and migration in human breast cancer MCF7 cells
Phosphorylation of myofibrillogenesis regulator-1 activates the MAPK signaling pathway and induces proliferation and migration in human breast cancer MCF7 cells
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DOI：
10.1016/j.febslet.2014.07.018
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发表时间：
2014-08-25
期刊：
影响因子：
3.5
通讯作者：
Shao, Rong-Guang
中科院分区：
文献类型：
--
作者：
Gong, Yuyan;He, Hongwei;Shao, Rong-Guang
肌原纤维生成调节因子-1(MR-1)在许多癌症中被认为是肿瘤促进剂。然而，其作用机制尚未完全阐明。在这里，我们报道了MR-1在人乳腺癌细胞中过表达，并通过激活ERK1/2信号通路参与了人乳腺癌MCF7细胞的促癌作用。MR-1与MEK1/2和ERK1相互作用，其N端序列在促进MEK/ERK级联反应中起主要作用。此外，还鉴定了MR-1的6个磷酸化位点，其中S46位的磷酸化对MEK/ERK的激活至关重要。因此，我们的研究结果表明，MR-1通过激活MEK/ERK信号而在MCF7细胞中作为肿瘤促进剂发挥作用。蛋白质相互作用结构概述：MR-1与ERK1通过反标签免疫共沉淀(View Interaction)物理相互作用(View Interaction)ERK1与MR-1通过反诱饵Coip(1，2)ERK1与MR-1物理相互作用(View Interaction)(C)2014欧洲生化学会联合会。爱思唯尔出版，版权所有。
Myofibrillogenesis regulator-1 (MR-1) has been characterized as a tumor promoter in many cancers. However, its mechanism of action has not been fully elucidated. Here, we report that MR-1 is over-expressed in human breast cancer cells and participates in tumor promotion in human breast cancer MCF7 cells by activating the ERK1/2 signaling pathway. MR-1 interacts with MEK1/2 and ERK1, and its N-terminal sequence plays a major role in promoting the MEK/ERK cascade. Furthermore, six phosphorylation sites of MR-1 were identified, and phosphorylation at S46 was shown to be critical for the activation of MEK/ERK. Therefore, our findings suggest that MR-1 functions as a tumor promoter in MCF7 cells by activating the MEK/ERK signaling.Structured summary of protein interactions:MR-1 physically interacts with ERK1 by anti tag coimmunoprecipitation (View interaction)ERK1 physically interacts with MR-1 by anti bait coip (1, 2)ERK1 and MR-1 colocalize by fluorescence microscopy (View interaction) (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.