Modulation of orphan nuclear receptor Nur77-mediated apoptotic pathway by acetylshikonin and analogues

Cancer Res. 2008 Nov 1;68(21):8871-80. doi: 10.1158/0008-5472.CAN-08-1972.

Abstract

Shikonin derivatives, which are the active components of the medicinal plant Lithospermum erythrorhizon, exhibit many biological effects including apoptosis induction through undefined mechanisms. We recently discovered that orphan nuclear receptor Nur77 migrates from the nucleus to the mitochondria, where it binds to Bcl-2 to induce apoptosis. Here, we report that certain shikonin derivatives could modulate the Nur77/Bcl-2 apoptotic pathway by increasing levels of Nur77 protein and promoting its mitochondrial targeting in cancer cells. Structural modification of acetylshikonin resulted in the identification of a derivative 5,8-diacetoxyl-6-(1'-acetoxyl-4'-methyl-3'-pentenyl)-1,4-naphthaquinones (SK07) that exhibited improved efficacy and specificity in activating the pathway. Unlike other Nur77 modulators, shikonins increased the levels of Nur77 protein through their posttranscriptional regulation. The apoptotic effect of SK07 was impaired in Nur77 knockout cells and suppressed by cotreatment with leptomycin B that inhibited Nur77 cytoplasmic localization. Furthermore, SK07 induced apoptosis in cells expressing the COOH-terminal half of Nur77 protein but not its NH(2)-terminal region. Our data also showed that SK07-induced apoptosis was associated with a Bcl-2 conformational change and Bax activation. Together, our results show that certain shikonin derivatives act as modulators of the Nur77-mediated apoptotic pathway and identify a new shikonin-based lead that targets Nur77 for apoptosis induction.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Anthraquinones / chemistry
  • Anthraquinones / pharmacology*
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Base Sequence
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Nucleus / metabolism
  • Cytoplasm / metabolism
  • DNA Primers
  • DNA-Binding Proteins / drug effects
  • DNA-Binding Proteins / metabolism
  • DNA-Binding Proteins / physiology*
  • Humans
  • Microscopy, Fluorescence
  • Mitochondria / metabolism
  • Nuclear Receptor Subfamily 4, Group A, Member 1
  • Protein Transport
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • RNA Processing, Post-Transcriptional / drug effects
  • Receptors, Steroid / drug effects
  • Receptors, Steroid / metabolism
  • Receptors, Steroid / physiology*
  • Reverse Transcriptase Polymerase Chain Reaction
  • bcl-2-Associated X Protein / metabolism

Substances

  • Anthraquinones
  • DNA Primers
  • DNA-Binding Proteins
  • NR4A1 protein, human
  • Nuclear Receptor Subfamily 4, Group A, Member 1
  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, Steroid
  • bcl-2-Associated X Protein
  • acetylshikonin