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目的研究过氧化物酶体增殖物激活受体γ(PPARγ)和肿瘤抑制基因PTEN在肝癌组织中表达的相关性,以及两种基因对人肝癌细胞BEL-7402细胞生长的影响,并探讨其机制。方法分别应用RT-PCR和Western blot观察分析肝癌组织、癌旁组织以及肝癌细胞中PPARγ和PTEN的表达情况;应用MTT法观察PPARγ的合成配体罗格列酮(RGZ)对BEL-7402细胞生长的影响。结果PPARγ mRNA和PTEN mRNA在肝癌组织较癌旁组织中表达是显著降低的,两者在肝癌组织中的表达呈正相关(r=0.774,P<0.01)。罗格列酮呈剂量和时间依赖性关系诱导PTEN蛋白的表达和抑制BEL-7402细胞的生长,此效应是通过PPARγ通路活化实现的。结论PPARγ和PTEN在肝癌中表达呈正相关,RGZ能够抑制BEL-7402细胞的生长,此效应与RGZ诱导PPARγ通路活化和PTEN表达上调有关。
Objective To investigate the correlation between the expression of peroxisome proliferator-activated receptor γ (PPARγ) and tumor suppressor gene PTEN in hepatocellular carcinoma and the effects of the two genes on the growth of human hepatocellular carcinoma cell BEL-7402, and to explore its mechanism. . Methods The expression of PPARγ and PTEN in hepatocellular carcinoma tissues, paracancerous tissues, and hepatocellular carcinomas were analyzed by RT-PCR and Western blot respectively. The growth of BEL-7402 cells was determined by MTT assay and the production of ligand PPARγ (RGZ) on BEL-7402 cells. Impact. Results The expressions of PPARγ mRNA and PTEN mRNA in hepatocellular carcinoma tissues were significantly lower than those in adjacent tissues. The expression of PPARγ mRNA and PTEN mRNA in hepatocellular carcinoma tissues was positively correlated (r=0.774, P<0.01). Rosiglitazone induced PTEN protein expression and inhibited the growth of BEL-7402 cells in a dose- and time-dependent manner. This effect was achieved through activation of the PPARγ pathway. Conclusion The expression of PPARγ and PTEN is positively correlated with hepatocellular carcinoma. RGZ can inhibit the growth of BEL-7402 cells. This effect is related to the activation of PPARγ pathway and up-regulation of PTEN expression induced by RGZ.