Targeting NF-κB and HIF-1 pathways for the treatment of cancer: part I

Arch Immunol Ther Exp (Warsz). 2011 Aug;59(4):289-99. doi: 10.1007/s00005-011-0131-4. Epub 2011 May 28.

Abstract

The process of chronic inflammation is a common link which connects different kinds of environmental pollutants and infections with tumorigenesis. Transcription factor NF-κB is a common final target for many inflammatory and cell proliferation pathways, independent of the source of stimuli (e.g., cytokines, growth factors, environmental carcinogens, radiation, hypoxia, bacteria, and viruses). Over-activation of NF-κB has been confirmed in many tumors, resulting in worse prognosis for patient survival. Therefore, inhibition of cellular pathways for NF-κB activation is nowadays considered as a promising anti-cancer therapy and is extensively studied in clinical trials, or even has been adopted as an approved therapy in some kinds of cancer.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Boronic Acids / pharmacology
  • Boronic Acids / therapeutic use
  • Bortezomib
  • Cell Line, Tumor
  • Cell Proliferation
  • Clinical Trials as Topic
  • Cytokines / metabolism
  • Gene Expression Regulation
  • Humans
  • Hypoxia-Inducible Factor 1 / antagonists & inhibitors
  • Hypoxia-Inducible Factor 1 / metabolism
  • Inflammation / drug therapy
  • Inflammation / genetics
  • Inflammation / physiopathology*
  • Mice
  • Models, Biological
  • NF-kappa B* / antagonists & inhibitors
  • NF-kappa B* / genetics
  • NF-kappa B* / metabolism
  • Neoplasms* / drug therapy
  • Neoplasms* / metabolism
  • Neoplasms* / physiopathology
  • Pyrazines / pharmacology
  • Pyrazines / therapeutic use
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Tumor Suppressor Protein p53 / agonists

Substances

  • Antineoplastic Agents
  • Boronic Acids
  • Cytokines
  • Hypoxia-Inducible Factor 1
  • NF-kappa B
  • Pyrazines
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Bortezomib