1. Peroxisome proliferator-activated receptor γ augments tumor necrosis factor family-induced apoptosis in hepatocellular carcinoma
- Author
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Takenari Yamanaka, Hiroshi Okano, Kazumoto Murata, Takahisa Sakai, Kazushi Sugimoto, Masatoshi Deguchi, Takeshi Nakano, Hidekazu Inoue, Katsuhiko Fujikawa, Shigeru Ohmori, and Katsuya Shiraki
- Subjects
Cancer Research ,Carcinoma, Hepatocellular ,Cellular differentiation ,Receptors, Cytoplasmic and Nuclear ,Peroxisome proliferator-activated receptor ,Apoptosis ,Biology ,Ligands ,TNF-Related Apoptosis-Inducing Ligand ,Tumor Cells, Cultured ,Humans ,Pharmacology (medical) ,fas Receptor ,Receptor ,Pharmacology ,chemistry.chemical_classification ,Membrane Glycoproteins ,Tumor Necrosis Factor-alpha ,Liver Neoplasms ,Nuclear Proteins ,Oncology ,chemistry ,Nuclear receptor ,Adipogenesis ,Cell culture ,Cancer research ,Tumor necrosis factor alpha ,Apoptosis Regulatory Proteins ,Cell Division ,Transcription Factors - Abstract
Proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor, which mainly associates with adipogenesis, but also appears to facilitate cell differentiation or apoptosis in certain malignant cells. This apoptosis induction by PPARgamma is increased by co-stimulation with tumor necrosis factor (TNF)-alpha-related apoptosis-inducing ligand (TRAIL), a member of the TNF family. In this study, we investigated the effect of PPARgamma on Fas-mediated apoptosis in hepatocellular carcinoma (HCC) cell lines. PPARgamma was expressed on all seven HCC cell lines and located in their nuclei. 15-Deoxy-Delta-12,14-prostaglandin J2 (15d- PGJ2), a PPARgamma ligand, inhibited cellular proliferation in HepG2, SK-Hep1 or HLE cells, unlike pioglitazone, another PPARgamma ligand, which did not have a significant influence on proliferation of these cells. However, 15d-PGJ2 facilitated Fas-mediated HCC apoptosis that could not be induced by Fas alone. These results suggest that PPARgamma can augment TNF-family-induced apoptosis.
- Published
- 2002
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