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Updated: Jun 19, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
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Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Neurotrophic receptor tyrosine kinase B induces c-fos-associated cell survival

Amiko Hayashi1, Kaname Nakatani, Junji Nishioka

  • 1Department of Molecular and Laboratory Medicine, Mie University Graduate School of Medicine, Mie, Japan.

International Journal of Molecular Medicine
|November 4, 2009
PubMed

Insights

Brain-derived neurotrophic factor (BDNF) binding to its receptor TrkB promotes cancer cell survival. This effect involves c-fos mRNA expression and is mediated by both MEK and PI3K pathways, highlighting TrkB

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Neurotrophic receptor tyrosine kinase B (TrkB) is a receptor for brain-derived neurotrophic factor (BDNF).
  • TrkB is expressed in various tumors and implicated in cellular processes.
  • Its precise intracellular functions, especially in cancer, require further elucidation.

Purpose of the Study:

  • To investigate the intracellular functions of TrkB using a stable 293T cell expression system.
  • To identify downstream target molecules and signaling pathways regulated by TrkB.
  • To understand TrkB's role in cell survival and its potential impact on tumorigenesis.

Main Methods:

  • Established 293T cells stably expressing human TrkB.
  • Utilized BDNF stimulation and TrkB inhibitors to assess cellular responses.
  • Investigated downstream signaling by measuring c-fos mRNA expression.
  • Employed specific inhibitors for mitogen-activated protein kinase (MEK) and phosphatidylinositol 3-kinase (PI3K) pathways.

Main Results:

  • BDNF stimulation of TrkB-expressing cells increased cell survival and c-fos mRNA expression.
  • TrkB inhibition completely abolished the BDNF-induced effects.
  • Combined MEK and PI3K inhibition partially reduced cell survival and c-fos mRNA levels.
  • Monotherapy with MEK or PI3K inhibitors did not significantly affect cell survival or c-fos mRNA expression.

Conclusions:

  • TrkB activation promotes cancer cell survival through c-fos mRNA expression.
  • The TrkB-mediated survival signaling involves both the MEK and PI3K pathways.
  • TrkB activation may significantly impact tumorigenesis and metastasis, suggesting therapeutic potential.

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