beta-Sitosterol inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle.
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.
Awad
A B
AB
Department of Physical Therapy, Exercise and Nutrition Sciences, SUNY/Buffalo, NY 14214, USA. awad@acsu.buffalo.edu
von Holtz
R L
RL
Cone
J P
JP
Fink
C S
CS
Chen
Y C
YC
D003110:Colonic Neoplasms / Q000473:pathology*; D006131:Growth Inhibitors / Q000494:pharmacology; D019073:HT29 Cells; D006801:Humans; D012855:Sitosterols / Q000494:pharmacology*; D013109:Sphingomyelins / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D010738:Type C Phospholipases / Q000378:metabolism
D006131:Growth Inhibitors; D012855:Sitosterols; D013109:Sphingomyelins; C025473:gamma-sitosterol; D010738:Type C Phospholipases