Induction of apoptosis by (-)-gossypol-enriched cottonseed oil in human breast cancer cells
Induction of apoptosis is one of the mechanisms of chemotherapeutic agents against breast cancer. In addition, recent studies have shown that diets containing polyphenolic components possess anticancer activities either in vitro or in vivo by inhibiting cell proliferation and inducing apoptosis. The...
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Published in | International journal of molecular medicine Vol. 26; no. 1; pp. 113 - 119 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Greece
D.A. Spandidos
01.07.2010
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Subjects | |
Online Access | Get full text |
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Summary: | Induction of apoptosis is one of the mechanisms of chemotherapeutic agents
against breast cancer. In addition, recent studies have shown that diets containing
polyphenolic components possess anticancer activities either in vitro or in vivo
by inhibiting cell proliferation and inducing apoptosis. The aim of our study
was to explore the effects of (-)-gossypol-enriched cottonseed oil [(-)-GPCSO],
a polyphenolic compound, on the proliferation of the breast cancer cell line MCF-7
as well as primary cultured human breast cancer epithelial cells (PCHBCEC). We
investigated whether the mechanism of the effects of (-)-GPCSO was mediated via
the induction of cell apoptosis and the regulation of Bcl-2 gene expression at
both the mRNA and protein levels. Our results showed that (-)-GPCSO inhibited
the proliferation of MCF-7 and PCHBCEC in a dose-dependent manner. (-)-GPCSO (0.1
and 0.2%) induced DNA fragmentation in both MCF-7 cells and PCHBCEC. (-)-GPCSO
suppressed the expression of Bcl-2 at both the mRNA and protein levels in MCF-7
cells and PCHBCEC in a dose-dependent fashion. Our results suggest that the growth
inhibitory effect of (-)-GPCSO on MCF-7 and PCHBCEC is due, at least partially,
to the induction of cell apoptosis, which is mediated by down-regulation of Bcl-2
expression at both the mRNA and protein levels. It might be possible for (-)-GPCSO
to be developed as a novel chemotherapeutic agent for breast cancer patients. |
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ISSN: | 1107-3756 1791-244X |
DOI: | 10.3892/ijmm_00000442 |