| The kinase defective EPHB6 receptor tyrosine kinase activates MAP kinase signaling in lung adenocarcinoma |
Authors: Jun Yu, Etmar Bulk, Ping Ji, Antje Hascher, Steffen Koschmieder, Wolfgang E. Berdel, Carsten Müller-Tidow |
Affiliations:
Department of Medicine, Hematology and Oncology, University of Münster, D-48129 Münster, Germany
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Doi: 10.3892/ijo_00000326 |
Pages: 175-179 |
Abstract:
Decreased expression levels of EPHB6, a member of the receptor tyrosine kinases (RTKs), are associated with an increased risk of metastasis development in early stage non-small cell lung cancer (NSCLC). However, the signaling properties of the kinase-defective EPHB6 receptor are not well-understood. Here, we show that expression of EPHB6 in A549 lung adenocarinoma cells led to phosphorylation of the MAP kinase ERK. Conversely, siRNA based knockdown of EPHB6 reversed ERK phosphorylation. Intriguingly, EPHB6-induced phosphorylation of ERK was uncoupled by activation of the Elk-1 transcriptional factor. These analyses suggest that kinase defective EPHB6 can lead to MAPK activation.
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