Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 499, Issue 4, Pages 920-926Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.04.020
Keywords
EphA2; ERK; Cell proliferation; Glioblastoma
Categories
Funding
- Ministry of Education, Science, Sports, and Culture of Japan [15K07043]
- Grants-in-Aid for Scientific Research [17J08982, 15K07043] Funding Source: KAKEN
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EphA2, a member of the Eph family of receptor tyrosine kinases, has been reported to promote tumor malignancy through phosphorylation of serine 897 (S897). Here, we found that overexpression of wild type EphA2 induced 5897 phosphorylation through ERK activation without growth factors or cytokines and promoted glioblastoma cell proliferation. However, overexpression of a kinase-inactive mutant of EphA2 failed to induce ERK activation, S897 phosphorylation, and promotion of glioblastoma cell proliferation. These data suggest that when overexpressed, EphA2 induces ERK activation through its tyrosine kinase activity, leading to 5897 phosphorylation and promotion of glioblastoma cell proliferation. Our findings provide a new insight into how EphA2 mediates glioblastoma progression. (C) 2018 Elsevier Inc. All rights reserved.
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