https://scholars.lib.ntu.edu.tw/handle/123456789/190777
Title: | Phosphorylation of LCRMP-1 by GSK3 beta Promotes Filopoda Formation, Migration and Invasion Abilities in Lung Cancer Cells | Authors: | Wang, Wen-Lung Hong, Tse-Ming Chang, Yih-Leong Wu, Chen-Tu Pan, Szu-Hua Yang, Pan-Chyr |
Issue Date: | 2012 | Journal Volume: | 7 | Journal Issue: | 2 | Start page/Pages: | - | Source: | PLoS One | Abstract: | LCRMP-1, a novel isoform of CRMP-1, can promote cancer cell migration, invasion and associate with poor clinical outcome in patients with non-small-cell lung cancer (NSCLC). However, the underlying regulatory mechanisms of LCRMP-1 in cancer cell invasiveness still remain obscure. Here, we report that GSK3 beta can phosphorylate LCRMP-1 at Thr-628 in consensus sequences and this phosphorylation is crucial for function of LCRMP-1 to promote filopodia formation, migration and invasion in cancer cells. Impediment of Thr-628 phosphorylation attenuates the stimulatory effects of LCRMP-1 on filopodia forming, migration and invasion abilities in cancer cells; simultaneously, kinase-dead GSK3 beta diminishes regulation of LCRMP-1 on cancer cell invasion. Furthermore, we also found that patients with low-level Ser-9-phosphorylated GSK3 beta expression and high-level LCRMP-1 expression have worse overall survival than those with high-level inactive GSK3 beta expressions and low-level LCRMP-1 expressions (P<0.0001). Collectively, these results demonstrate that GSK3 beta-dependent phosphorylation of LCRMP-1 provides an important mechanism for regulation of LCRMP-1 on cancer cell invasiveness and clinical outcome. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/259771 |
Appears in Collections: | 醫學系 |
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