Abstract
The anti-tumor effect of non-steroidal anti-inflammatory drugs (NSAIDs) remains unclear. Here, we found that the susceptibility for NSAIDs-induced apoptosis might correlate with the status of the p53 gene in gastric cancer cells. Apoptosis in gastric cancer cells expressing wild-type p53 is induced through up-regulation of bax and down-regulation of bcl-2 and that regulation of the bax-bcl-2 heterodimer may be a major target of NSAIDs. As to gastric cancer cells expressing mutant-type p53, other key factors may exist in the NSAIDs' growth inhibition action.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
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Antineoplastic Agents / pharmacology*
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Apoptosis* / genetics
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Aspirin / pharmacology
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Cell Line, Tumor
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Dimerization
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Down-Regulation
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Drug Resistance, Neoplasm*
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Humans
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Indomethacin / pharmacology
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Mutation
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Stomach Neoplasms / genetics
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Stomach Neoplasms / metabolism*
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Stomach Neoplasms / pathology
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism*
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Up-Regulation
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bcl-2-Associated X Protein / metabolism
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Antineoplastic Agents
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Proto-Oncogene Proteins c-bcl-2
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Tumor Suppressor Protein p53
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bcl-2-Associated X Protein
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Aspirin
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Indomethacin