Effect of chemopreventive agents on glutathione S-transferase P1-1 gene expression mechanisms via activating protein 1 and nuclear factor kappaB inhibition

Annelyse Duvoix, Sylvie Delhalle, Romain Blasius, Michaël Schnekenburger, Franck Morceau, Marjorie Fougère, Estelle Henry, Marie Madeleine Galteau, Mario Dicato, Marc Diederich*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

71 Citations (Scopus)

Abstract

Glutathione S-transferase P1-1 (GSTP1-1) is a phase II drug metabolism enzyme implicated in carcinogenesis and development of resistance to anti-cancer drugs. It was previously shown that both activating protein 1 (AP-1) and nuclear factor κB (NF-κB) are involved in its regulation. In the present study we examined the inhibitory effect of several chemopreventive agents on the tumor necrosis factor (TNF) α- or 12-O-tetradecanoylphorbol 13 acetate (TPA)-induced promoter activity of GSTP1-1, as demonstrated by transient transfection experiments in K562 and U937 leukemia cells. Our results provide evidence for a differential effect of chemopreventive agents such as β-lapachone, emodin, sanguinarine and capsaicin, which significantly inhibit reporter gene expression as well as TNFα- and TPA-induced binding of AP-1 and NF-κB, whereas trans-anethole and silymarin do not produce any inhibitory effect. Our results demonstrate the ability of selected chemopreventive agents to decrease GSTP1-1 gene expression mechanisms and could thus contribute to reduce the incidence of glutathione related drug resistance in human leukemia.

Original languageEnglish
Pages (from-to)1101-1111
Number of pages11
JournalBiochemical Pharmacology
Volume68
Issue number6
DOIs
Publication statusPublished - 15 Sept 2004
Externally publishedYes

Keywords

  • 12-O-tetradecanoylphorbol 13 acetate
  • AP-1
  • Carcinogenesis
  • Chemopreventive agents
  • Drug resistance
  • GST
  • GSTP1-1
  • Leukemia
  • NF-κB
  • TNFα
  • TPA
  • activating protein 1
  • glutathione S-transferase
  • nuclear factor κB
  • tumor necrosis α

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