beta-Sitosterol inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle

Anticancer Res. Jan-Feb 1998;18(1A):471-3.

Abstract

The present study examined the SM cycle as a mechanism to explain the inhibitory effect of SIT on HT-29 cell growth. SIT was the main phytosterol in the diet. Supplementation of SIT at 16 microM for 5 days in the media inhibited growth by 55% as compared to cholesterol. SIT supplementation had no effect on sphingosine production. Ceramide production increased 45% with SIT supplementation as compared to cholesterol. Sterol supplementation had no effect on phospholipase C, a key enzyme in the PKC pathway. We concluded that the activation of the SM cycle may play a role in growth inhibition of HT-29 cells by SIT.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Colonic Neoplasms / pathology*
  • Growth Inhibitors / pharmacology
  • HT29 Cells
  • Humans
  • Sitosterols / pharmacology*
  • Sphingomyelins / metabolism*
  • Tumor Cells, Cultured
  • Type C Phospholipases / metabolism

Substances

  • Growth Inhibitors
  • Sitosterols
  • Sphingomyelins
  • gamma-sitosterol
  • Type C Phospholipases