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目的观察过氧化物酶体增殖物激活型受体γ(PPARγ)配体15-脱氧-前列腺素J2 (15-d-PGJ2)对MGC803胃癌细胞体外黏附和侵袭转移能力的影响。方法免疫荧光细胞化学法检测PPARγ蛋白表达,噻唑蓝(MTT)比色法检测15-d-PGJ2对胃癌细胞黏附的影响,体外侵袭实验检测其对胃癌细胞侵袭和趋化能力的影响。结果PPARγ主要定位于细胞核;15-d-PGJ2在1、10μmol/L水平上明显抑制细胞的黏附(P均<0.05);对胃癌细胞的侵袭和趋化能力有明显抑制作用(P值均<0.05),抑制率分别为38.32%、56.60%和47.83%、61.69%,具有剂量依赖关系。结论MGC803表达功能性PPARγ蛋白。PPARγ可能是治疗胃癌的新靶点,15-d-PGJ2可能是治疗胃癌的有效试剂。
Objective To observe the effect of 15-deoxy-prostaglandin J2 (15-d-PGJ2), a ligand of peroxisome proliferator-activated receptor γ (PPARγ), on the adhesion, invasion and metastasis of gastric cancer MGC803 cells in vitro. Methods The expression of PPARγ protein was detected by immunofluorescence cytochemistry. The effect of 15-d-PGJ2 on the adhesion of gastric cancer cells was detected by MTT assay. The invasion and chemotactic ability of gastric cancer cells were detected by in vitro invasion assay. Results PPARγ mainly localized in the nucleus. 15-d-PGJ2 significantly inhibited cell adhesion at the concentration of 1 and 10 μmol / L (all P <0.05), and inhibited gastric cancer cell invasion and chemotaxis (P < 0.05). The inhibition rates were 38.32%, 56.60% and 47.83%, 61.69%, respectively, in a dose-dependent manner. Conclusion MGC803 expresses functional PPARγ protein. PPARγ may be a new target for the treatment of gastric cancer, 15-d-PGJ2 may be an effective agent for the treatment of gastric cancer.