Mechanism underlying the epidermal growth factor-mediated nuclear translocation of NF-κB in glioblastoma U-87MG cells

VernacularTitle:表皮生长因子介导成胶质瘤细胞NF-κB核转位的机制初探
Author: Ting PAN ¹ ; Zhi-Peng ZOU ; Jun LIN ; Shen-Qiu LUO
Author Information

1. 南方医科大学
Keywords: Glioblastoma; NF-κB; PLCγ1; PKCα
From: Chinese Journal of Neuromedicine 2008;7(4):333-337
CountryChina
Language:Chinese
Abstract: Objective To investigate the mechanisms by which nuclear factor-κB (NF-κB)translocates to nucleus of human glioblastoma U-87MG cells. Methods The levels of NF-κB translocating to nucleus in U-87MG after activation or inhibition ofphospholipase C-γ1 (PLCγ1) were first determined by electrophoretic mobility shift assay (EMSA), and then the levels of NF-κBtranslocating to nucleus in U-87MG after activation or inhibition of protein kinase-α (PKCα) were determined by EMSA. Results The level of NF- κB translocating to nucleus of U-87MG peaked 60min after EGF stimulation, which could be reversed by the pretreatment of PLCγ1 specific inhibitor U-73122. Moreover, PKC specific agonist phorbol myristate acetate (PMA) stimulation for 60 min promoted the nuclear translocation of NF-κB to the peak, which could be also effectively reversed by the pre-treatment of PKCα specific antagonist Ro 31-8220. Conclusions Epidermal growth factor can mediate the nuclear translocation of NF-κB in U-87MG through the signal transduction of PLCγ1-PKCα,thereby regulating the transcription of related invasion and metastasis genes.