Hypoxia and inflammation in Cancer, focus on HIF and NF-κB

Laura D'Ignazio, Michael Batie, Sonia Rocha (Lead / Corresponding author)

Research output: Contribution to journalReview articlepeer-review

67 Citations (Scopus)
137 Downloads (Pure)

Abstract

Abstract: Cancer is often characterised by the presence of hypoxia and inflammation. Paramount to the mechanisms controlling cellular responses under such stress stimuli, are the transcription factor families of Hypoxia Inducible Factor (HIF) and Nuclear Factor of kappa-light-chain-enhancer of activated B cells (NF-κB). Although, a detailed understating of how these transcription factors respond to their cognate stimulus is well established, it is now appreciated that HIF and NF-κB undergo extensive crosstalk, in particular in pathological situations such as cancer. Here, we focus on the current knowledge on how HIF is activated by inflammation and how NF-κB is modulated by hypoxia. We summarise the evidence for the possible mechanism behind this activation and how HIF and NF-κB function impacts cancer, focusing on colorectal, breast and lung cancer. We discuss possible new points of therapeutic intervention aiming to harness the current understanding of the HIF-NF-κB crosstalk.
Original languageEnglish
Article number21
Number of pages23
JournalBiomedicines
Volume5
Issue number2
DOIs
Publication statusPublished - 9 May 2017

Keywords

  • NF-κB
  • Hypoxia
  • Inflammation
  • IKK
  • PHDs
  • Cancer
  • TAK1
  • FIH

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