MED28 regulates MEK1-dependent cellular migration in human breast cancer cells

HuangC.-Y.; ChouY.-H.; HsiehN.-T.ChenH.-H.LeeM.-F.

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MED28 regulates MEK1-dependent cellular migration in human breast cancer cells

机译：MED28调节MEK1-dependent细胞迁移在人类乳腺癌细胞

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MED28, a mammalian Mediator subunit, exhibits several cellular roles, including a merlin, Grb2, and cytoskeleton-associated protein (magicin), a repressor of smooth muscle cell differentiation, and an endothelial-derived gene (EG-1). Overexpression of MED28 may stimulate cell proliferation which presumably results from the transcriptional activation of the Mediator function. Additionally, several tumors, including breast cancer, highly express MED28. We have found recently that MED28 potentiated epidermal growth factor (EGF)-induced migration in human breast cancer cells. Therefore, the objective of this study is to identify the role of MED28 in the aspect of cellular migration and invasion in human breast cancer cells. Suppression of MED28 blocked cellular migration and invasion with concomitant reduced expression levels of matrix metalloproteinase-2 (MMP2) and mitogen-activated protein kinase kinase 1 (MAP2K1; MEK1); overexpression of MED28 enhanced cellular migration and upregulated MMP2 and MEK1 expression. Moreover, suppression of MEK1, by dominant-negative, kinase-dead MEK1 cDNA construct or MEK1-specific small interfering RNA (siRNA) as well as MEK1 inhibitors, blocked MED28-induced MMP2 activation, cellular migration, and invasion in breast cancer cells. Furthermore, ectopic expression of MEK1 rescued the inhibitory effect of MED28 knockdown on invasion, and exogenous MMP2 recombinant protein recovered the suppression on invasion upon MED28 or MEK1 knockdown. Our data indicate that MED28 regulates cellular migration in a MEK1-dependent manner in human breast cancer cells, reinforcing the important cellular roles of MED28.

机译：哺乳动物中介单元MED28,展品几个细胞的角色,包括一个梅林,Grb2和cytoskeleton-associated蛋白质(magicin)平滑肌细胞分化抑制因子,和一个endothelial-derived基因(EG-1)。超表达MED28可能刺激细胞扩散的可能的结果转录激活的中介函数。乳腺癌、高度表达MED28。最近发现MED28强表皮全身的生长因子(EGF)在人类迁移乳腺癌细胞。本研究旨在确定MED28的作用细胞迁移和入侵的方面人类乳腺癌细胞。阻止了细胞迁移和入侵伴随矩阵的表达水平metalloproteinase-2 (MMP2)和增殖作用蛋白激酶激酶1 (MAP2K1;MED28增强细胞的过度迁移和调节MMP2和MEK1表达式。显性负,kinase-dead MEK1互补脱氧核糖核酸构造或MEK1-specific小干扰RNA(siRNA)以及MEK1抑制剂,屏蔽MED28-induced MMP2激活,细胞乳腺癌细胞迁移和入侵。此外,异位表达MEK1获救MED28击倒的抑制作用入侵,外生MMP2重组蛋白质恢复的抑制MED28入侵或MEK1击倒。MEK1-dependent调节细胞迁移的方式在人类乳腺癌细胞,加强重要的细胞MED28的角色。

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来源
《Journal of Cellular Physiology》 |2012年第12期|3820-3827|共8页
作者
HuangC.-Y.; ChouY.-H.; HsiehN.-T.ChenH.-H.LeeM.-F.;
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作者单位

Department of Nutrition, China Medical University, Taichung, Taiwan;

Department of Nutrition and Health Sciences, Chang Jung Christian University, Tainan, Taiwan;

Department of Nutritional Science, Fu Jen Catholic University, Taipei, Taiwan;

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正文语种英语
中图分类细胞生物学;
关键词
Breast Cancer Cell; MAP2K1 gene; Cell MigrationCell LocomotionInvasionsSmooth muscle cellMediator ComplexBreast Cancercell invasionMitogen Activated Protein Kinase Kinase 1;

机译：乳腺癌细胞;MAP2K1基因;细胞MigrationCellLocomotionInvasionsSmooth肌肉cellMediatorComplexBreast Cancercell invasionMitogen激活蛋白激酶激酶1;

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MED28 regulates MEK1-dependent cellular migration in human breast cancer cells

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