Abstract
Treatment of MIN mice with the nonsteroidal anti-inflammatory drug, nabumetone, resulted in a dose-dependent suppression of intestinal tumorigenesis. In both the uninvolved MIN mouse colonic epithelium and HT-29 colon cancer cells, nabumetone downregulated the anti-apoptotic protein, Bcl-2, with concomitant induction of apoptosis, suggesting a potential mechanism for colon cancer chemoprevention.
Copyright 2001 Cancer Research Campaign.
MeSH terms
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Adenomatous Polyposis Coli / genetics
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Anticarcinogenic Agents / pharmacology*
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Apoptosis / drug effects*
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Butanones / pharmacology*
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Colonic Neoplasms / pathology
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Colonic Neoplasms / prevention & control
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Disease Models, Animal
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Gene Expression Regulation*
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Genes, bcl-2*
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Humans
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Intestinal Neoplasms / genetics
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Intestinal Neoplasms / pathology
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Intestinal Neoplasms / prevention & control*
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Mice
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Mice, Mutant Strains
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Nabumetone
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Tumor Cells, Cultured
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Anticarcinogenic Agents
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Butanones
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Proto-Oncogene Proteins c-bcl-2
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Nabumetone