MCC, a new interacting protein for Scrib, is required for cell migration in epithelial cells

被引:25
|
作者
Arnaud, Camille [1 ,2 ,3 ]
Sebbagh, Michael [1 ,2 ,3 ]
Nola, Sebastien [1 ,2 ,3 ]
Audebert, Stephane [1 ,2 ,3 ]
Bidaut, Ghislain [1 ,2 ,3 ]
Hermant, Aurelie [1 ,2 ,3 ]
Gayet, Odile [4 ,5 ]
Dusetti, Nelson J. [4 ,5 ]
Ollendorff, Vincent [6 ]
Santoni, Marie-Josee [1 ,2 ,3 ]
Borg, Jean-Paul [1 ,2 ,3 ]
Lecine, Patrick [1 ,2 ,3 ]
机构
[1] Ctr Rech Cancerol Marseille, INSERM, UMR891, F-13009 Marseille, France
[2] Inst J Paoli I Calmettes, F-13009 Marseille, France
[3] Univ Mediterranee, F-13007 Marseille, France
[4] INSERM, U624, F-13258 Marseille, France
[5] Aix Marseille Univ, Marseille, France
[6] INRA, UMR Differentiat Cellulaire & Croissance 866, F-34060 Montpellier, France
来源
FEBS LETTERS | 2009年 / 583卷 / 14期
关键词
Cell migration; Protein interaction; Tumor suppressor; COLORECTAL-CANCER; TUMOR-SUPPRESSOR; BETA-CATENIN; GENETIC SCREEN; E6; PROTEINS; E-CADHERIN; DROSOPHILA; POLARITY; CHROMOSOME-5Q21; IDENTIFICATION;
D O I
10.1016/j.febslet.2009.06.034
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To further characterize the molecular events supporting the tumor suppressor activity of Scrib in mammals, we aim to identify new binding partners. We isolated MCC, a recently identified binding partner for beta-catenin, as a new interacting protein for Scrib. MCC interacts with both Scrib and the NHERF1/NHERF2/Ezrin complex in a PDZ-dependent manner. In T47D cells, MCC and Scrib proteins colocalize at the cell membrane and reduced expression of MCC results in impaired cell migration. By contrast to Scrib, MCC inhibits cell directed migration independently of Rac1, Cdc42 and PAK activation. Altogether, these results identify MCC as a potential scaffold protein regulating cell movement and able to bind Scrib, beta-catenin and NHERF1/2.
引用
收藏
页码:2326 / 2332
页数:7
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