Edimo William's Elong, Ramos Ana Raquel, Ghosh Somadri, Vanderwinden Jean-Marie, Erneux Christophe
IRIBHM, Université Libre de Bruxelles, Campus Erasme, Bâtiment C, 808 Route de Lennik, B-1070, Bruxelles, Belgium.
Neurophysiology Lab, Université Libre de Bruxelles, Campus Erasme, Bâtiment C, 808 Route de Lennik, B-1070, Bruxelles, Belgium.
Biochem Biophys Res Commun. 2016 Aug 5;476(4):508-514. doi: 10.1016/j.bbrc.2016.05.154. Epub 2016 May 28.
The phosphoinositide 5-phosphatases consist of several enzymes that have been shown to modulate cell migration and invasion. SHIP2, one family member, is known to interact with growth factor receptors and cytoskeletal proteins. In a human model of glioblastoma 1321 N1 cells, we recently identified Myo1c as a new interactor of SHIP2. This was shown in a complex of proteins also containing filamin A. We show here that SHIP2 localization at lamellipodia and ruffles is impaired in Myo1c depleted cells. In the absence of Myo1c, N1 cells tend to associate to form clusters. Cell migration is very much reduced in Myo1c depleted cells, concomitantly with a decrease in FAK Tyr397 phosphorylation, focal adhesion length and PI(4,5)P2 immunostaining. In N1 cells, Myo1c is thus important for lamellipodia formation to assemble a protein complex containing SHIP2 to facilitate cell migration.
磷酸肌醇5 - 磷酸酶由几种已被证明可调节细胞迁移和侵袭的酶组成。SHIP2是其中一个家族成员，已知它能与生长因子受体和细胞骨架蛋白相互作用。在胶质母细胞瘤1321 N1细胞的人类模型中，我们最近鉴定出Myo1c是SHIP2的一个新相互作用蛋白。这在一个还包含细丝蛋白A的蛋白质复合物中得到了证实。我们在此表明，在Myo1c缺失的细胞中，SHIP2在片状伪足和微绒毛处的定位受损。在没有Myo1c的情况下，N1细胞倾向于聚集形成细胞簇。Myo1c缺失的细胞中细胞迁移显著减少，同时FAK Tyr397磷酸化、粘着斑长度和PI(4,5)P2免疫染色也减少。因此，在N1细胞中，Myo1c对于形成包含SHIP2的蛋白复合物以促进细胞迁移的片状伪足形成很重要。
