Structure-activity studies of the indole alkaloid tumor promoter teleocidins

Carcinogenesis. 1987 Apr;8(4):547-52.

Abstract

New teleocidin derivatives with various substituents at positions 2, 5 and 7 of the indole ring were prepared from (-)-indolactam V, which is the fundamental structure of teleocidins and has a tumor-promoting activity, to examine the contribution of the alkyl substituents of teleocidins to the activity. Their possible tumor-promoting activities in vivo were evaluated by Epstein-Barr virus early antigen-inducing activity and inhibition of specific binding of [3H]TPA to a mouse epidermal particulate fraction. These two biological activities correlated well for each derivative. Large substituents at positions 2 and 5 remarkably lowered the activities, indicating that the structural requirements for the activities of these domains are especially strict. To investigate in detail the contribution of position 2 of (-)-indolactam V to the activities, new microbial metabolites, (-)-2-oxy-indolactam V, and blastmycetin B and C, were also tested. These compounds proved to be inactive, suggesting that the double bond at position 2 plays an important role for the activities. Substituents at position 7 generally enhanced the activities and even blastmycetin A, which is a dimer of (-)-indolactam V, showed high activities. The effects of the substituents on binding ability to the 12-O-tetradecanoylphorbol-13-acetate receptor were analyzed quantitatively using physicochemical substituent parameters and regression analysis. The results exhibited the fact that hydrophobicity of the substituents plays a critical role for receptor binding, and supported the hypothesis that the monoterpenoid moiety of teleocidins is involved in the non-specific hydrophobic interaction with phospholipids in cell membrane.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Viral / biosynthesis
  • Caenorhabditis elegans Proteins*
  • Carcinogens*
  • Carrier Proteins
  • Lyngbya Toxins / toxicity*
  • Mice
  • Protein Kinase C*
  • Receptors, Drug*
  • Receptors, Immunologic / metabolism
  • Regression Analysis
  • Structure-Activity Relationship
  • Tetradecanoylphorbol Acetate / metabolism

Substances

  • Antigens, Viral
  • Caenorhabditis elegans Proteins
  • Carcinogens
  • Carrier Proteins
  • Epstein-Barr virus early antigen
  • Lyngbya Toxins
  • Receptors, Drug
  • Receptors, Immunologic
  • phorbol ester binding protein
  • phorbol ester receptor
  • teleocidins
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate