%0 Journal Article
%T Peroxisome proliferator-activated receptor-¦Ã is essential in the pathogenesis of gastric carcinoma
%A Xiu-Mei Ma
%A Hong Yu
%A Na Huai
%J World Journal of Gastroenterology
%D 2009
%I Baishideng Publishing Group Co. Limited
%X AIM: To investigate whether peroxisome proliferator-activated receptor ¦Ã (PPAR-¦Ã) is expressed in human gastric carcinoma and whether PPAR-¦Ã is a potential target for gastric carcinoma therapy.METHODS: PPAR-¦Ã protein in gastric carcinoma was examined by immunohistochemistry. In the gastric carcinoma cell line MGC803, PPAR-¦Ã, survivin, Skp2 and p27 protein and mRNA were examined by Western blotting and real-time reverse transcription-polymerase chain reaction, respectively; proliferation was examined by MTT; apoptosis was examined by chromatin staining with Hoechst 33342 and fluorescence activated cell sorting (FACS). and cell cycle was examined by FACS; the knockdown of PPAR-¦Ã was done by RNA interference.RESULTS: A high level of expression of PPAR-¦Ã was observed in human gastric carcinoma and in a human gastric carcinoma cell line MGC803. The PPAR-¦Ã agonist 15-deoxy-¦¤12,14-prostaglandin J2 (15d-PGJ2) inhibited growth, and induced apoptosis and G1/G0 cell cycle arrest in MGC803 cells in a concentration-dependent and time-dependent manner. The effect of 15d-PGJ2 on MGC803 cells was not reversed by the selective and irreversible antagonist GW9662 for PPAR-¦Ã. Furthermore, survivin and Skp2 expression were decreased, whereas p27 expression was enhanced following 15d-PGJ2 treatment in a dose-dependent manner in MGC803 cells. Interestingly, we also found that small interfering RNA for PPAR-¦Ã inhibited growth and induced apoptosis in MGC803 cells. The inhibition of PPAR-¦Ã function may be a potentially important and novel modality for treatment and prevention of gastric carcinoma.CONCLUSION: A PPAR-¦Ã agonist inhibited growth of human gastric carcinoma MGC803 cells by inducing apoptosis and G1/G0 cell cycle arrest with the involvement of survivin, Skp2 and p27 and not via PPAR-¦Ã.
%K Peroxisome proliferator-activated receptor ¦Ã
%K Gastric cancer
%K Apoptosis
%K Cell cycle
%U http://www.wjgnet.com/1007-9327/full/v15/i31/3874.htm