Indirubin-3'-monoxime, a derivative of a Chinese anti-leukemia medicine, inhibits Notch1 signaling

Cancer Lett. 2008 Jul 8;265(2):215-25. doi: 10.1016/j.canlet.2008.02.013. Epub 2008 Mar 17.

Abstract

Notch proteins perform a critical function in cell-fate decisions and in differentiation. In this study, we determined that indirubin-3'-monoxime reduced Notch1 signaling to a remarkable extent. Indirubin-3'-monoxime has been shown to inhibit both constitutive active mutants of Notch1 and Notch1-IC-mediated transactivation activity. However, in such cases, neither the Notch cleavage pattern nor the protein stability of Notch1-IC was determined to have been significantly altered. Indirubin-3'-monoxime suppresses Notch1 transcriptional activity via the dissociation of the Notch1-IC-RBP-Jk complex. Notably, the transcriptional activity of Notch1-IC was not suppressed significantly in the GSK-3beta null cells by indirubin-3'-monoxime as compared to what was observed with GSK-3beta wild-type cells. In the previous study, we synthesized a series of indirubin derivatives. Interestingly, some of these indirubin derivatives were characterized as potent inhibitors of Notch1 signaling. Taken together, the results of this study indicate that indirubin-3'-monoxime downregulated Notch1 signaling in a GSK-3beta-dependent and proteosomal degradation-independent manner.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Down-Regulation
  • Embryonic Stem Cells / drug effects
  • Embryonic Stem Cells / metabolism*
  • Glycogen Synthase Kinase 3 / metabolism
  • Humans
  • Indoles / pharmacology*
  • Oximes / pharmacology*
  • Protein Structure, Tertiary
  • Receptors, Notch / metabolism*
  • Signal Transduction / drug effects

Substances

  • Indoles
  • Oximes
  • Receptors, Notch
  • indirubin-3'-monoxime
  • Glycogen Synthase Kinase 3