5'-Nitro-indirubinoxime inhibits epidermal growth factor- and phorbol ester-induced AP-1 activity and cell transformation through inhibition of phosphorylation of Pin1

Mol Carcinog. 2011 Dec;50(12):961-71. doi: 10.1002/mc.20761. Epub 2011 Mar 11.

Abstract

5'-Nitro-indirubinoxime (5'-NIO), a derivative of indirubin, exhibits anti-cancer activity in a variety of human cancer cells. However, the underlying molecular mechanisms and molecular target(s) of the chemopreventive activities of 5'-NIO remain unknown. Here, we report that 5'-NIO inhibited the epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced neoplastic cell transformation of JB6 Cl41 mouse skin epidermal cells without any cytotoxic effects. Western blot analysis revealed that 5'-NIO inhibited activities of Raf-1 (S338), MEK1/2, ERK1/2, JNK, and c-Jun induced by EGF or TPA, respectively, whereas it did not affect autophosphorylation of epidermal growth factor receptor (EGFR) induced by EGF or TPA. In addition, 5'-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Importantly, 5'-NIO inhibited Pin1 phosphorylation at serine 16 induced by EGF or TPA, respectively, resulted in the inhibition of interaction between Pin1 and Raf-1. Immunoprecipitation/immunoblot analysis revealed that 5'-NIO bound with Pin1. Together, these findings suggest that 5'-NIO might act as an anticarcinogene in EGF- or TPA-induced carcinogenesis through the inhibition of interaction between Pin1 and Raf-1. © 2011 Wiley Periodicals, Inc.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticarcinogenic Agents / pharmacology*
  • Cell Line
  • Cell Transformation, Neoplastic / drug effects*
  • Epidermal Growth Factor / pharmacology*
  • Indoles / pharmacology*
  • JNK Mitogen-Activated Protein Kinases / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Signaling System / drug effects
  • Mice
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Oximes / pharmacology*
  • Peptidylprolyl Isomerase / metabolism*
  • Phosphorylation
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism
  • Proto-Oncogene Proteins c-raf / antagonists & inhibitors
  • Proto-Oncogene Proteins c-raf / metabolism
  • Tetradecanoylphorbol Acetate / pharmacology*
  • Transcription Factor AP-1 / antagonists & inhibitors
  • Transcription Factor AP-1 / metabolism*
  • Transcription, Genetic / drug effects
  • Transcriptional Activation / drug effects

Substances

  • 5'-nitroindirubinoxime
  • Anticarcinogenic Agents
  • Indoles
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Oximes
  • Proto-Oncogene Proteins c-fos
  • Transcription Factor AP-1
  • Epidermal Growth Factor
  • Proto-Oncogene Proteins c-raf
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • PIN1 protein, human
  • Peptidylprolyl Isomerase
  • Pin1 protein, mouse
  • Tetradecanoylphorbol Acetate