Activation of the aryl hydrocarbon receptor by TCDD inhibits senescence: A tumor promoting event?

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53 Scopus citations


Activation of the aryl hydrocarbon receptor (AHR) by the agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to promote tumor formation in both liver and skin. In the liver, but not the skin, the AHR-mediated events that contribute to TCDD's tumor promoting activities have been studied in some detail and are thought to involve perturbation of cell fate processes. However, studies performed using cultured cells have often resulted in apparent contradictory results indicating that the impact of TCDD on cell fate processes may be cell context dependent. We and others have shown that in primary cultured keratinocytes TCDD increases post-confluent proliferation and increases late differentiation. Further, our studies performed in these cells indicate that TCDD can also inhibit culture-induced senescence. While senescence, a permanent cell cycle arrest, is emerging as an important process regulated by oncogenes and considered to be of therapeutic importance, its role with respect to TCDD/AHR mediated tumor promotion has not been fully considered. The intent of this article is to focus primarily on senescence as a cell process relevant to skin tumorigenesis and explore the idea that the inhibition of senescence by TCDD could be an important mechanism by which it may exert its tumor promoting effects in the skin.

Original languageEnglish
Pages (from-to)681-688
Number of pages8
JournalBiochemical Pharmacology
Issue number4
StatePublished - Feb 15 2009


  • 2,3,7,8-Tetrachlorodibenzo-p-dioxin
  • Aryl hydrocarbon receptor
  • Keratinocytes
  • Senescence
  • Tumorigenesis

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology


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