Synergistic cytotoxicity exhibited by combination treatment of selective retinoid ligands with taxol (Paclitaxel)

Cancer Res. 2001 Dec 15;61(24):8703-11.

Abstract

The focus of this study was to develop retinoic acid receptor (RAR) RAR alpha/beta selective agonists with anticancer efficacy and reduced toxicity associated with RAR gamma activity. In these studies, we report the identification and characterization of high-affinity RAR alpha/beta selective agonists with limited RAR gamma activity. These compounds inhibited human tumor cell line proliferation with similar efficacy to that observed for a pan-RAR agonist. However, for most tumor cell lines, the efficacy of these compounds was restricted to the micromolar range. To determine whether the RAR alpha/beta selective agonists could be additive or synergistic with existing agents, we investigated the effects of combining RAR alpha/beta selective agonists with various cytotoxic agents. Our results showed that the alpha/beta selective retinoids dramatically lowered the effective dose of Taxol needed to induce cytotoxicity of a wide range of tumor cell lines. This synergy was specific to tubulin-modifying agents and could not be observed with a variety of other cytotoxic agents of diverse function. Examination of pathways common to Taxol and retinoid signaling revealed that this synergy was related in part to effects on Bcl-2 expression/phosphorylation as well as the activity of the c-Jun NH(2)-terminal kinase and activator protein-1. In contrast, the tubulin polymerization induced by Taxol was not further affected by cotreatment with a variety of retinoid receptor ligands. These observations indicate that potent RAR alpha/beta selective agonists may be of therapeutic benefit in combination with Taxol therapy.

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Apoptosis / drug effects
  • Cell Division / drug effects
  • Drug Synergism
  • Growth Inhibitors / administration & dosage
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism
  • Paclitaxel / administration & dosage
  • Paclitaxel / pharmacology*
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Receptors, Retinoic Acid / agonists*
  • Retinoic Acid Receptor alpha
  • Retinoids / administration & dosage
  • Retinoids / pharmacology*
  • Substrate Specificity
  • Transcription Factor AP-1 / metabolism
  • Transcriptional Activation / drug effects
  • Tubulin / metabolism
  • Tumor Cells, Cultured

Substances

  • Growth Inhibitors
  • Proto-Oncogene Proteins c-bcl-2
  • RARA protein, human
  • Rara protein, mouse
  • Receptors, Retinoic Acid
  • Retinoic Acid Receptor alpha
  • Retinoids
  • Transcription Factor AP-1
  • Tubulin
  • retinoic acid receptor beta
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • Paclitaxel