The kinase defective EPHB6 receptor tyrosine kinase activates MAP kinase signaling in lung adenocarcinoma

Jun Yu; Etmar Bulk; Ping Ji; Antje Hascher; Steffen Koschmieder; Wolfgang E. Berdel; Carsten Müller-Tidow

doi:10.3892/ijo_00000326

The kinase defective EPHB6 receptor tyrosine kinase activates MAP kinase signaling in lung adenocarcinoma

Jun Yu, Etmar Bulk, Ping Ji, Antje Hascher, Steffen Koschmieder, Wolfgang E. Berdel, Carsten Müller-Tidow

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

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.

Original language	English (US)
Pages (from-to)	175-179
Number of pages	5
Journal	International journal of oncology
Volume	35
Issue number	1
DOIs	https://doi.org/10.3892/ijo_00000326
State	Published - 2009
Externally published	Yes

Keywords

EPHB6
Elk-1
Extracellular-signal-regulated kinase
Mitogen-activated protein kinase
Non-small cell lung cancer
Receptor tyrosine kinase

ASJC Scopus subject areas

Oncology
Cancer Research

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10.3892/ijo_00000326

Cite this

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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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AU - Yu, Jun

AU - Bulk, Etmar

AU - Ji, Ping

AU - Hascher, Antje

AU - Koschmieder, Steffen

AU - Berdel, Wolfgang E.

AU - Müller-Tidow, Carsten

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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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The kinase defective EPHB6 receptor tyrosine kinase activates MAP kinase signaling in lung adenocarcinoma

Abstract

Keywords

ASJC Scopus subject areas

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