PPARγ ligand‐induced apoptosis through a p53‐dependent mechanism in human gastric cancer cells

We have recently demonstrated that the PPARγ ligand troglitazone induced cell growth arrest and evoked apoptosis in a gastric cancer cell line, MKN–45. Since in general, p53 plays an important role in the induction of apoptosis and growth inhibition, we tried to clarify whether or not p53 mediates t...

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Bibliographic Details
Published in:	Cancer science Vol. 94; no. 4; pp. 338 - 343
Main Authors:	Nagamine, Miho, Okumura, Toshikatsu, Tanno, Satoshi, Sawamukai, Mitsuko, Motomura, Wataru, Takahashi, Nobuhiko, Kongo, Yutaka
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-04-2003 Blackwell John Wiley & Sons, Inc
Subjects:	Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Biological and medical sciences Bisphenol A Cell Cycle Proteins - metabolism Cell Division - drug effects Cell growth Chromans - pharmacology Cyclin-Dependent Kinase Inhibitor p27 DNA-Binding Proteins - metabolism Gastric cancer Gastroenterology. Liver. Pancreas. Abdomen Genes, Dominant Humans Ligands Medical sciences Mutants p53 Protein Receptors, Cytoplasmic and Nuclear - metabolism Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Thiazolidinediones - pharmacology Transcription Factors - metabolism Transfection Troglitazone Tumor Cells, Cultured - metabolism Tumor Cells, Cultured - pathology Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumor Suppressor Proteins - metabolism Tumors Human Stomach Nuclear receptor Malignant tumor PPAR-γ receptor TP53 Gene Cell death Established cell line Digestive diseases Genetics Gastric disease Apoptosis Tumor suppressor gene Hormonal receptor
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