PPAR-γ及CTGF对肝癌细胞生长的影响及相互作用的研究

Influence of PPAR-γ and CTGF on growth of hepatocellular carcinoma cells and correlation of both factors

目的过氧化物酶体增殖物激活受体-γ(PPARγ)及结缔组织生长因子(CTGF)对肿瘤细胞的生物学行为都有一定的影响,本文旨在探讨二者对肝癌细胞生长的影响及二者之间的关系。方法培养人肝癌细胞HepG-2,经不同浓度、不同时间的PPAR-γ激动剂罗格列酮(RGZ)及CTGF抗体封闭处理后,MTT法检测细胞活力,博依登小室测定细胞侵袭及迁移特性的改变。RT-PCR检测经RGZ处理前后CTGF mRNA表达的变化。结果罗格列酮及CTGF抗体处理后肝癌细胞的增殖均受抑制,且呈时间和剂量依赖性,同时细胞的侵袭、迁移能力也受到抑制。且经RGZ处理后,CTGF mRNA的表达较处理前下降。结论PPAR-γ和CTGF都可以影响肝癌细胞的增殖、侵袭及迁徙能力,PPAR-γ调控肝癌细胞的生长部分是通过调控CTGF的表达来实现的。

【Objective】To investigate the influence of peroxisome proliferator-activated receptor-γ （PPAR-γ） and connective tissue growth factor （CTGF） on hepatocellular carcinoma cell growth and their correlation because both factors play an important role in the biological behaviour of hepatocellular carcinoma （HepG2） cells【.Methods】HepG2 cells were treated with the ligand of PPARγrosiglitazone （RGZ）and antibody of CTGF at different concentrations for different periods. The proliferation of HepG2 cells was assessed by MTT assay. The changes of invasion and immigration of HepG2 cells were detected by Boyden chamber assay. The expression of CTGF mRNA after treatment of rosiglitazone was detected by RT-PCR. 【Results】MTT assay demonstrated that rosiglitazone had inhibitory effect on the proliferation of HepG2 cells in a timeand dosedependent manner, and CTGF also had the same effect. The invasion and immigration of HepG2 cells were inhibited, too. RT-PCR demonstrated that the expression of CTGF mRNA in PPARγ-treated cells was down-regulated compared with the control group.【Conclusion】The ligand of PPARγrosiglitazone and antibody of CTGF could inhibit the proliferation of HepG2 cells. The mechanism of PPAR-γ regulating the growth of HCC cells may be associated with regulation of CTGF expression