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PPAR-gamma ligands inhibit growth of human esophageal adenocarcinoma cells through induction of apoptosis, cell cycle arrest and reduction of ornithine decarboxylase activity.
- Source :
-
International journal of oncology [Int J Oncol] 2001 Sep; Vol. 19 (3), pp. 465-71. - Publication Year :
- 2001
-
Abstract
- Peroxisome proliferator-activated receptor gamma (PPAR-gamma), a member of the nuclear hormone receptor superfamily, is involved in suppression of growth of several types of tumors such as liposarcoma, breast cancer, prostate cancer, and colon cancer, possibly through induction of cell cycle arrest and/or apoptosis. In this study, we demonstrated expression of PPAR-gamma mRNA and protein in human esophageal carcinoma cells. Expression of PPAR-gamma protein was higher in an adenocarcinoma cell line (TE-7 cells) than in a squamous cell carcinoma cell line (TE-1 cells). PPAR-gamma ligands such as 15-deoxy-Delta12,14-prostaglandin J2 and troglitazone significantly inhibited the growth of TE-7 cells but had less or no effect on growth of TE-1 cells. 15d-PGJ2 and troglitazone induced apoptosis in TE-7 cells but not in TE-1 cells. Troglitazone caused G1 cell cycle arrest and reduced ornithine decarboxylase activity (ODC) in TE-7 cells but not in TE-1 cells. Inhibition by PPAR-gamma ligands of growth of esophageal adenocarcinoma cells may thus be due to induction of apoptosis, G1 cell cycle arrest and reduction of ODC activity.
- Subjects :
- Adenocarcinoma pathology
Antineoplastic Agents pharmacology
Blotting, Western
Carcinoma, Squamous Cell metabolism
Carcinoma, Squamous Cell pathology
Cell Division drug effects
Chromans pharmacology
DNA Primers chemistry
Esophageal Neoplasms pathology
Flow Cytometry
Humans
Immunologic Factors pharmacology
Ligands
Prostaglandin D2 analogs & derivatives
RNA, Messenger metabolism
Receptors, Cytoplasmic and Nuclear metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tetrazolium Salts
Thiazoles pharmacology
Thymidine chemistry
Transcription Factors metabolism
Troglitazone
Tumor Cells, Cultured drug effects
Tumor Cells, Cultured physiology
Adenocarcinoma metabolism
Apoptosis drug effects
Cell Cycle drug effects
Esophageal Neoplasms metabolism
Ornithine Decarboxylase metabolism
Prostaglandin D2 pharmacology
Receptors, Cytoplasmic and Nuclear genetics
Thiazolidinediones
Transcription Factors genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1019-6439
- Volume :
- 19
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- International journal of oncology
- Publication Type :
- Academic Journal
- Accession number :
- 11494023