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 journalArticlepeer-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 languageEnglish (US)
Pages (from-to)175-179
Number of pages5
JournalInternational journal of oncology
Volume35
Issue number1
DOIs
StatePublished - 2009

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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