BUFFALO, N.Y. -- A plant-based fat abundant in vegetarian diets and shown to inhibit the growth of prostate and colon cancer cells in vitro, also inhibits the growth in vitro of one line of breast-cancer cells, University at Buffalo nutrition researchers have found.
The study, presented at the annual meeting of the Federation of American Societies of Experimental Biology earlier this month, showed that the phytosterol B-sitosterol reduced the number of breast-cancer cells grown in a laboratory setting by 66 percent, compared to controls.
"These results go hand-in-hand with our findings on prostate and colon cancer," said Atif Awad, Ph.D., director of UB's Nutrition Program and senior researcher on the study. He noted, however, that researchers haven't identified how B-sitosterol inhibits breast-cancer cell growth, but they do know it does not appear to be the same mechanism that is at work in prostate and colon cancer cells. "The effect of B-sitosterol apparently varies with the type of tissue," Awad said.
Awad is an associate professor in the Department of Physical Therapy, Exercise and Nutrition Sciences in the UB School of Health Related Professions.
He and colleagues at UB have been trying to understand the mechanisms responsible for vegetarians' lower rates of hormone-dependent cancers, and for the lower mortality rate from such cancers in Asian countries, where populations eat little meat.
With fats known to play a role in the development of several cancers, Awad's group has been focusing on the phytosterols for possible answers. He reported at an international conference on cancer research in Greece last October that the phytosterol B-sitosterol appears to play a role in inhibiting the growth of human prostate-cancer cells by strengthening an intracellular signaling system that inhibits cell division.
An earlier study by Awad published in 1998 in the Journal of Nutritional Biochemistry reported that plant-based fats may cut the risk of prostate cancer by reducing the levels of testosterone and certain enzymes that metabolize testosterone into more active forms.
"If we know how phytosterols work, we can advise people how to modify their diets to reduce their risk of cancers, or we could eventually design drugs to target systems they influence," Awad noted. "Meanwhile, these findings reinforce the importance of including large amounts of vegetables in the diet."
In the current work, Awad's research team examined the effect of B-sitosterol and another prevalent plant fat, campesterol, on the growth of a particular line of estrogen-independent breast cancer cells, designated MDA-MB-231. Cell cultures were supplemented with either of the two plant fats or cholesterol. A control culture received no supplementation.
Cell counts after five days showed that cultures supplemented with B-sitosterol had 66 percent fewer breast-cancer cells than controls or cultures supplemented with cholesterol or campesterol. B-sitosterol had no effect on the activity of an enzyme called PP2A, which was found in his previous study to play a role in reducing prostate-cancer cell growth.
Additional researchers on the study were A. Downie, UB graduate student in nutrition, and Carol S. Fink, Ph.D., UB clinical assistant professor of nutrition.