Carcinogenesis, Vol 18, 229-232, Copyright © 1997 by Oxford University Press
M Mandal, X Wu and R Kumar
Epidemiological studies have linked dietary fiber to the prevention of
human colorectal cancer and suggest that short chain fatty acids such as
butyric acid, which is produced by fermentation of dietary fiber in the
large intestine, may be an important mediator of the protective effects of
fiber. We investigated the role of Bcl-2 deregulation on the sensitivity of
colorectal carcinoma cells to undergo butyrate-induced apoptosis. Here we
report an inverse relationship between the levels of Bcl-2 and the
sensitivity of colorectal carcinoma cell lines to undergo apoptosis in
response to butyrate. Overexpression of Bcl-2 in colorectal carcinoma DiFi
cells resulted in suppression of butyrate- induced apoptosis and enhanced
cell survival in response to butyrate. Butyrate-induced apoptosis was
accompanied by inhibition of expression of a 30 kDa protein (p30,
immunorecognized by anti-Bcl-2 mAb) and this cellular effect of butyrate
was inhibited by Bcl-2 overexpression. These findings suggest that
deregulation of Bcl-2 in human colorectal carcinoma cells confers
resistance to induction of apoptosis by butyrate, a dietary micronutrient.
ARTICLES
Bcl-2 deregulation leads to inhibition of sodium butyrate-induced apoptosis in human colorectal carcinoma cells
Department of Medicine, Pennsylvania State University College of Medicine, Hershey 17033, USA.
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