Dd. Taylor et al., MODULATION OF COLON-TUMOR ONCOGENE EXPRESSION BY CANCER PATIENT-DERIVED LIPIDS, Journal of surgical oncology, 63(1), 1996, pp. 46-51
In an effort to understand the role of specific fats on carcinogenesis
, we have studied the effects of lipids derived from cancer patients o
n components associated with the regulation of proliferation. The trea
tment of tumor cells with patient-derived fats produced increased cell
proliferation, as indicated by shorter doubling times. The effects of
patient-derived lipids on the expression of ras, c-jun, c-erbB-2, and
p53 gene products were examined. The cellular expression of the ras p
roto-oncogene product was increased in both colon tumor cell lines, fo
llowing lipid treatment. However, c-jun proto-oncogene expression was
elevated in HT-29 cells and appeared unchanged in SK-Co-1 cells after
lipid treatment. Treatment of HT-29 tumor cells with patient-derived f
ats produced an enhancement of the p53 gene product, whereas fat treat
ment reduced p53 expression in SK-Co-1 tumor cells. Further separation
of the patient-derived fats indicated that the amplification of p53 g
ene expression in HT-29 cells could be achieved primarily by addition
of the diacylglycerides fraction. Addition of the purified fatty acids
, comprising the diglyceride fraction, indicated that the fatty acids,
16:1, 18:0, and 18:1, induced the most significant increases in p53 e
xpression by HT-29 cells. These alterations caused by cancer patient-d
erived fats are consistent with the loss of normal growth regulation a
nd may explain the epidemiologic association between certain fats and
carcinogenesis. (C) 1996 Wiley-Liss, Inc.