【摘 要】
：
Increased transcriptional activity of-catenin resulting from Wnt/Wingless-dependent or-independent signaling has been detected in many types of human cancer
【机 构】
：
Department of Neuro-Oncology University of Texas MD Anderson Cancer Center Houston, TX USA
【出 处】
：
BIT‘s2nd Annual World Cancer Congess-2009 (2009第二届癌症大会)
论文部分内容阅读
Increased transcriptional activity of-catenin resulting from Wnt/Wingless-dependent or-independent signaling has been detected in many types of human cancer, but the underlying mechanism of Wnt-independent regulation remains unclear.We demonstrate here that EGFR activation results in disruption of the cormplex of-catenin and-catenin, thereby abrogating the inhibitory effect of-catenin on-catenin transactivation via CK2-dependent phosphorylation of-catenin.ERK2, which is activated from EGFR signaling, directly binds to CK2 via the ERK2 docking groove and phosphorylates CK2 and subsequently enhanced CK2 activity toward-catenin phosphorylation.In addition, levels of ERK1/2 activity are correlated with levels of-catenin phosphorylation at Ser641 in human glioblastoma specimens.This EGFR-ERK-CK2-mediated phosphorylation of-catenin promotes-catenin transactivation and tumor cell invasion.
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