论文部分内容阅读
目的:探讨过氧化物酶体激活物活化受体γ(peroxisome proliferator-activated receptor gamma,PPARγ)活化在诱导人胃癌MGC803细胞周期停滞中的作用。方法:MTT法检测吡格列酮(pioglitazone,PGZ)对MGC803细胞增殖的抑制作用;流式细胞术检测肿瘤细胞周期的改变;RT-PCR方法检测PPARγ、细胞周期蛋白Cyclin D1和细胞周期蛋白依赖性激酶CDK4的表达。结果:0.1~10μmol/L PGZ作用MGC803细胞96 h后能显著抑制细胞增殖;10μmol/L PGZ分别作用48、72和96 h,G1期细胞随着作用时间的延长而增加,呈明显的G1期阻滞;在MGC803细胞中PPARγ表达较弱,经10μmol/L PGZ作用48 h表达水平显著增加;作用96 h,细胞中细胞周期调节因子CDK4表达显著降低(P<0.01),Cyclin D1轻微下调。结论:PPARγ活化能诱导MGC803细胞周期G1期阻滞,该作用可能与其下调细胞周期因子CDK4和Cyclin D1的表达有关。
Objective: To investigate the role of peroxisome proliferator-activated receptor gamma (PPARγ) activation in the induction of cell cycle arrest in human gastric cancer MGC803 cells. Methods: MTT assay was used to detect the inhibitory effect of pioglitazone (PGZ) on the proliferation of MGC803 cells. The changes of tumor cell cycle were detected by flow cytometry. The expressions of PPARγ, cyclin D1 and cyclin D1 expression. Results: After treated with 0.1 ~ 10μmol / L PGZ, MGC803 cells could significantly inhibit cell proliferation 96 h after treatment with 10μmol / L PGZ for 48, 72 and 96 h, respectively. The cells in G1 phase increased with the prolongation of G1 phase, The expression of PPARγ in MGC803 cells was weak. The expression of PPARγ in MGC803 cells was significantly increased after 48 h treatment with 10 μmol / L PGZ. The expression of CDK4 was down-regulated significantly (P <0.01) and Cyclin D1 was down-regulated slightly in 96 h. CONCLUSION: Activation of PPARγ induces G1 phase arrest in MGC803 cells, which may be related to its down-regulation of the expression of CDK4 and Cyclin D1.