Susceptibility for NSAIDs-induced apoptosis correlates to p53 gene status in gastric cancer cells.
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.
Zhang
Yan-Jie
YJ
Digestive Department of the No. 3 People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Dai
Qiang
Q
Wu
Shu-Ming
SM
Zhu
Hong-Yin
HY
Shen
Guan-Feng
GF
Li
En-Ling
EL
Xiao
Shu-Dong
SD
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000235:genetics; D001241:Aspirin / Q000494:pharmacology; D045744:Cell Line, Tumor; D019281:Dimerization; D015536:Down-Regulation; D019008:Drug Resistance, Neoplasm; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D009154:Mutation; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000970:Antineoplastic Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D001241:Aspirin; D007213:Indomethacin