A novel indole ethyl isothiocyanate (7Me-IEITC) with anti-proliferative and pro-apoptotic effects on platinum-resistant human ovarian cancer cells

Gynecol Oncol. 2008 May;109(2):240-9. doi: 10.1016/j.ygyno.2008.01.042. Epub 2008 Mar 7.

Abstract

Objective: A novel indole ethyl isothiocyanate derivative (7Me-IEITC) was defined as a potent growth-suppressing agent to cell lines derived from ovarian cancers. Key mechanisms of the cellular response in vitro were studied and suggest a potential of 7Me-IEITC as a therapeutic drug.

Methods: The viability of ovarian cancer cell lines (SKOV-3, OVCAR-3) in comparison to pancreatic and prostate cancer cell lines, primary fibroblast and immortalized trophoblasts after treatment with 7Me-IEITC was analyzed. Morphological and apoptotic responses of SKOV-3 were studied by fluorescence microscopy (DAPI staining, TUNEL assay). SKOV-3 proliferation was estimated by a standardized BrdU incorporation assay. The phosphorylation of MAP-Kinases, pro-survival factors and the activation of caspases and PARP-1 were analyzed by western blotting. Changes of the mitochondrial transmembrane-potential and in cell-cycle progression were studied by FACS analysis. MAP-Kinase and caspase inhibitors were employed in cytotoxicity studies.

Results: 7Me-IEITC selectively reduced the viability of SKOV-3, OVCAR-3, BXPC-3 and PC-3 cells (IC(50) values < or = 5 microM), while the viability of fibroblasts or trophoblasts remained un-affected at concentrations below 20 microM. 7Me-IEITC treatment down-regulated pro-survival kinases and transcription factors (STAT-3, IKKalpha and NF-kappaB), caused rapid loss of the mitochondrial transmembrane-potential and inactivation of PARP-1 along with activation of caspases. The use of p38 MAP-Kinase-and caspase inhibitors suppressed the cytotoxicity of the drug. 7Me-IEITC acted as an anti-proliferative agent and arrested the cell-cycle progression of SKOV-3 in G2/M phase.

Conclusion: 7Me-IEITC is a potent and growth-suppressing agent to cell lines derived from ovarian cancers by causing deactivation of survival signals, apoptosis, and cell-cycle arrest.

Publication types

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

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Adenocarcinoma / physiopathology*
  • Apoptosis / drug effects*
  • Biomarkers / metabolism
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cell Survival / drug effects
  • Drug Resistance, Neoplasm
  • Enzyme Activation / drug effects
  • Female
  • Humans
  • Indoles / pharmacology*
  • Isocyanates / pharmacology*
  • Male
  • Membrane Potential, Mitochondrial / drug effects
  • Mitogen-Activated Protein Kinases / metabolism
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology
  • Ovarian Neoplasms / physiopathology*
  • Pancreatic Neoplasms / pathology
  • Pancreatic Neoplasms / physiopathology
  • Platinum / pharmacology*
  • Prostatic Neoplasms / pathology
  • Prostatic Neoplasms / physiopathology

Substances

  • 7-methyl-indole ethyl isothiocyanate
  • Biomarkers
  • Indoles
  • Isocyanates
  • Platinum
  • Mitogen-Activated Protein Kinases