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CT-GF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。
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 pe- riods. The proliferation of HepG-2 cells was assessed by MTT.The change of invasion and immigration of HepC--2 cells were detected by boyden. The rnRNA level of CTGF in HepG2 cells treated with rosiglitazone was detected by RT-PCR. Results HepG-2 cells express CTGF and PPAR-y 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 ros- iglitazone. 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.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2009年第1期36-39,共4页
Cancer Research on Prevention and Treatment
