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Linking JNK Activity to the DNA Damage Response

Vincent Picco1, Gilles Pagès2

  • 1Biomedical Research Department, Centre Scientifique de Monaco, Nice, France.

Genes & Cancer
|December 19, 2013
PubMed

Insights

DNA breaks trigger c-Jun N-terminal kinase (JNK) activation via NF-κB and TNF-α signaling. This review details the pathway and its implications for DNA-damaging cancer therapies.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Cancer Research

Background:

  • c-Jun N-terminal kinase (JNK) activation was initially linked to UV radiation and oncogenes.
  • JNK activation is also induced by various DNA-damaging agents like gamma irradiation and chemotherapy.
  • Recent studies reveal a pathway connecting DNA breaks to JNK activation.

Purpose of the Study:

  • To review the pathway initiated by physical DNA breaks leading to JNK activation.
  • To discuss the cellular consequences of this JNK activation.
  • To explore the implications for cancer therapy using DNA-damaging agents.

Main Methods:

  • Literature review of studies on JNK activation pathways.
  • Focus on the pathway initiated by DNA helix breakage.
  • Analysis of NF-κB, TNF-α, and autocrine JNK signaling.

Main Results:

  • Physical DNA breaks activate the transcription factor NF-κB.
  • NF-κB activation leads to TNF-α secretion.
  • TNF-α mediates autocrine JNK pathway activation.

Conclusions:

  • DNA damage response pathways involving JNK are crucial for cellular outcomes.
  • Understanding this pathway can inform the development of more effective DNA-damaging cancer therapies.
  • Targeting JNK signaling may enhance treatment efficacy.
Keywords:
DNA damageJNKUV irradiation

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