title: PPAR-gamma ligands inhibit growth of human esophageal adenocarcinoma cells through induction of apoptosis, cell cycle arrest and reduction of ornithine decarboxylase activity.
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.
authors.affiliation: Department of Biochemistry, Osaka City University Medical School, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan. d98m011@medsv2.med.osaka-cu.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Takashima
authors.forename: Y
authors.initials: Y
authors.lastname: Fujiwara
authors.forename: K
authors.initials: K
authors.lastname: Higuchi
authors.forename: T
authors.initials: T
authors.lastname: Arakawa
authors.forename: Y
authors.initials: Y
authors.lastname: Yano
authors.forename: T
authors.initials: T
authors.lastname: Hasuma
authors.forename: S
authors.initials: S
authors.lastname: Otani
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000473:pathology; D002453:Cell Cycle / Q000187:drug effects*; D002455:Cell Division / Q000187:drug effects; D002839:Chromans / Q000494:pharmacology; D017931:DNA Primers / Q000737:chemistry; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D005434:Flow Cytometry; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology; D008024:Ligands; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D015230:Prostaglandin D2 / Q000031:analogs & derivatives / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013778:Tetrazolium Salts; D013844:Thiazoles / Q000494:pharmacology; D045162:Thiazolidinediones; D013936:Thymidine / Q000737:chemistry; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism; D000077288:Troglitazone; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000502:physiology
chemical_list: C097240:15-deoxy-delta(12,14)-prostaglandin J2; D000970:Antineoplastic Agents; D002839:Chromans; D017931:DNA Primers; D007155:Immunologic Factors; D008024:Ligands; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D013778:Tetrazolium Salts; D013844:Thiazoles; D045162:Thiazolidinediones; D014157:Transcription Factors; D009955:Ornithine Decarboxylase; C022616:thiazolyl blue; D000077288:Troglitazone; D015230:Prostaglandin D2; D013936:Thymidine