title: Combinational effect of PPARγ agonist and RXR agonist on the growth of SGC7901 gastric carcinoma cells in vitro.
abstract: In order to investigate the inhibitory effects and mechanisms of troglitazone (TGZ), a peroxisome proliferator-activated receptor γ (PPARγ) agonist, and retinoid X receptor (RXR) agonist (9-cis-retinoic acid (RA)) on gastric carcinoma cells SGC7901, SGC7901 cells were treated with TGZ and 9-cis-RA, respectively, or in combination. Then, the cell growth, apoptosis, morphological changes, and the expression of PPARγ, RXRγ, Bcl-2, and Bax were detected by MTT assay, flow cytometry, HE staining, immunocytochemistry staining, and Western blot assay, respectively. Our results showed that the growth of SGC7901 cells was inhibited and the cells got sparser at the concentrations of 50 μmol/L TGZ, 20 μmol/L 9-cis-RA, or combination of TGZ (25 μmol/L) and 9-cis-RA (10 μmol/L). Immunocytochemistry and Western blot showed that after 72 h, the expression of PPARγ, RXRγ, and Bax were upregulated; Bcl-2 was downregulated compared with the negative control group. These data indicated that PPARγ agonist and RXR agonist could inhibit the proliferation of SGC7901 cells via inducing the apoptosis, which involved the increase in the level of Bax/Bcl-2. The combination of RXR agonist and PPARγ agonist could induce the maximal inhibitory effects on tumor growth and apoptosis via promoting the formation of RXR/PPARγ heterodimer.
authors.affiliation: Department of Pathology, Xuzhou Medical College, Xuzhou, 221002, People's Republic of China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Zu-an
authors.initials: ZA
authors.lastname: Zhu
authors.forename: Shang-Nuan
authors.initials: SN
authors.lastname: Zhang
authors.forename: Jie
authors.initials: J
authors.lastname: Mou
authors.forename: Lei
authors.initials: L
authors.lastname: Liu
authors.forename: Tao
authors.initials: T
authors.lastname: Cui
authors.forename: Dong-Sheng
authors.initials: DS
authors.lastname: Pei
mesh_terms: D000077556:Alitretinoin; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002839:Chromans / Q000494:pharmacology*; D015536:Down-Regulation; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007364:Intercalating Agents / Q000494:pharmacology; D047495:PPAR gamma / Q000819:agonists* / Q000096:biosynthesis; D011419:Propidium / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D047488:Retinoid X Receptors / Q000819:agonists* / Q000096:biosynthesis; D013274:Stomach Neoplasms / Q000188:drug therapy*; D045162:Thiazolidinediones / Q000494:pharmacology*; D014212:Tretinoin / Q000494:pharmacology*; D000077288:Troglitazone; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis
chemical_list: D000970:Antineoplastic Agents; D002839:Chromans; D007004:Hypoglycemic Agents; D007364:Intercalating Agents; D047495:PPAR gamma; D019253:Proto-Oncogene Proteins c-bcl-2; D047488:Retinoid X Receptors; D045162:Thiazolidinediones; D051028:bcl-2-Associated X Protein; D000077556:Alitretinoin; D011419:Propidium; D014212:Tretinoin; D000077288:Troglitazone