NDLI: EphA2 is a key effector of the MEK/ERK/RSK pathway regulating glioblastoma cell proliferation

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EphA2 is a key effector of the MEK/ERK/RSK pathway regulating glioblastoma cell proliferation

Content Provider	Scilit
Author	Hamaoka, Yuho Negishi, Manabu Katoh, Hironori
Copyright Year	2016
Description	Journal: Cellular Signalling EphA2, a member of the Eph receptor tyrosine kinases, is frequently overexpressed in a variety of malignancies, including glioblastoma, and its expression is correlated with poor prognosis. EphA2 acts as a tumor promoter through a ligand ephrin-independent mechanism, which requires phosphorylation of EphA2 on serine 897 (S897), leading to increased cell migration and invasion. In this study, we show that ligand-independent EphA2 signaling occurs downstream of the MEK/ERK/RSK pathway and mediates epidermal growth factor (EGF)-induced cell proliferation in glioblastoma cells. Suppression of EphA2 expression by long-term exposure to ligand ephrinA1 or EphA2-targeted shRNA inhibited EGF-induced cell proliferation. Stimulation of the cells with EGF induced EphA2 S897 phosphorylation, which was suppressed by MEK and RSK inhibitors, but not by phosphatidylinositol 3-kinase (PI3K) and Akt inhibitors. The RSK inhibitor or RSK2-targeted shRNA also suppressed EGF-induced cell proliferation. Furthermore, overexpression of wild-type EphA2 promoted cell proliferation without EGF stimulation, whereas overexpression of EphA2-S897A mutant suppressed EGF- or RSK2-induced proliferation. Taken together, these results suggest that EphA2 is a key downstream target of the MEK/ERK/RSK signaling pathway in the regulation of glioblastoma cell proliferation.
Related Links	https://repository.kulib.kyoto-u.ac.jp/dspace/bitstream/2433/230208/1/j.cellsig.2016.04.009.pdf
Ending Page	945
Page Count	9
Starting Page	937
ISSN	08986568
e-ISSN	18733913
DOI	10.1016/j.cellsig.2016.04.009
Journal	Cellular Signalling
Issue Number	8
Volume Number	28
Language	English
Publisher	Elsevier BV
Publisher Date	2016-08-01
Access Restriction	Open
Subject Keyword	Journal: Cellular Signalling Biochemistry and Molecular Biology Cell Proliferation
Content Type	Text
Resource Type	Article
Subject	Cell Biology

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