CTGF对肝癌细胞生物学行为的影响及其与PPAR-γ关系的探讨
Influence of CTGF on Hepatocellular Carcinoma Cells and Correlation with PPAR-γ
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摘要: 目的 探讨结缔组织生长因子（CTGF/CCN2）对肝癌细胞生物学行为的调控作用，及其与PPAR-γ在肝癌中的相互关系。 方法 免疫组织化学法检测HepG-2细胞中CTGF及PPAR-γ蛋白的表达。经不同浓度、不同时间的CTGF抗体封闭处理人肝癌细胞HepG-2后,MTT法测定细胞活力,博依登小室测定细胞侵袭及迁移特性的改变。经PPAR-γ激动剂(rosiglitazone,罗格列酮)处理HepG-2细胞后， RT-PCR 检测CTGF mRNA表达的改变。 结果 HepG-2细胞表达CTGF及PPAR-γ蛋白。肝癌细胞经CTGF抗体处理后，其增殖受抑制,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。HepG-2 细胞经罗格列酮处理后，其CTGF mRNA的表达下降。 结论 CTGF可以调控肝癌细胞的增殖、侵袭及迁移能力。PPAR-γ调控肝癌细胞的生长，部分是通过改变CTGF的表达来实现的。Abstract: Objective To investigate the effect of connective tissue growth factor (CTGF/CCN2) on the growth of human hepatocellular carcinoma cells, and explore the correlation between PPAR-γ and CTGF. Methods The expression of CTGF and PPAR-γ protein in HepG-2 cell was detected by immunohistochemistry.HepG-2 cells treated with the antibody of CTGF, at different concentrations for different periods. The proliferation of HepG-2 cells was assessed by MTT. The change of invasion and immigration of HepG-2 cells were detected by boyden. The mRNA level of CTGF in HepG-2 cells treated with rosiglitazone was detected by RT-PCR. Results HepG-2 cells express CTGF and PPAR-γ protein. MTT assay demonstrated that antibody of CTGF had inhibitory effect on the proliferation of HepG-2 cells in a time-and dose-dependent manner.The invasion and immigration of HepG-2 cells were inhibited,too. The result of RT-PCR demonstrated that the mRNA level of CTGF was down-regulated after treated with rosiglitazone. Conclusion The antibody of CTGF could inhibit the proliferation, invasion and immigration of HepG-2 cells. The mechanism of PPAR-γ regulating the growth of HCC cell may be associated with down-regulating the expression of CTGF.
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