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胆管上皮细胞株抑制共培养的肝癌HepG2细胞株增殖
何瑶1*,黄文生2,杨荣萍1,任明1
0
(1.中山大学附属第一医院消化科,广州 510080;;2.中山大学附属第一医院外科,广州 510080)
摘要:
目的通过体外共培养肝内胆管上皮细胞株(mIBEC)与肝癌细胞株HepG2,探讨mIBEC对HepG2细胞株的可能作用。方法体外共培养HepG2与mIBEC,采用CellTiter 96R○ AQueous One Solution Cell Proliferation Assay 分别测定并比较HepG2细胞单独培养时以及与mIBEC共培养后增殖的情况;实时定量PCR法分别测定HepG2细胞单独培养时以及与mIBEC共培养后其Ki67及caspase3 mRNA表达水平;蛋白质免疫印迹法分别测定HepG2细胞单独培养时以及与mIBEC共培养后其caspase3蛋白表达水平。结果与mIBEC共培养后24~72 h,HepG2细胞增殖水平低于其单独培养时的水平(P<0.01),且伴有Ki67 mRNA表达的下调(P<0.05);与mIBEC共培养后,HepG2细胞caspase3 mRNA及蛋白表达水平较其单独培养时均上调,差异有统计学意义(P<0.05)。结论mIBEC可抑制共培养的HepG2细胞增殖; caspase3激活表达上调可能是mIBEC抑制共培养的HepG2细胞增殖的机制之一。
关键词:  肝肿瘤  胆管上皮细胞  HepG2细胞  共培养  caspase3  细胞凋亡
DOI:10.3724/SP.J.1008.2011.017
投稿时间:2010-09-14修订日期:2010-10-28
基金项目:广东省自然科学基金(4009383).
Biliary epithelial cells inhibit proliferation of co-cultured hepatic cancer cell line HepG2
HE Yao1*,HUANG Wen-sheng2,YANG Rong-ping1,REN Ming1
(1. Department of Gastroenterology, the First Affiliated Hospital of SUN Yat-sen University, Guangzhou 510080, Guangdong, China;;2. Department of Surgery, the First Affiliated Hospital of SUN Yat-sen University, Guangzhou 510080, Guangdong, China)
Abstract:
ObjectiveTo investigate the possible effect of mouse intrahepatic biliary epithelial cell line (mIBEC) on cocultured human hepatoma cell lines HepG2.MethodsHepG2 and mIBEC cells were cocultured in a membraneseparated Transwell system. CellTiter 96R○ AQueous One Solution Cell Proliferation Assay (Promega Corporation,Madison,WI) was used to examine HepG2 cell proliferation in the system with or without cocultured mIBEC. Realtime PCR(RTPCR)was used to determine Ki67 and caspase3 mRNA expression in HepG2 cells in a system with or without cocultured mIBEC. Western blotting analysis was used to determine caspase3 protein level in HepG2 cells. ResultsThe proliferation of the cocultured HepG2 cells was significantly lower than those cultured alone(P<0.01). Expression of Ki67,a cell proliferation marker,was also significantly downregulated in mIBEC cocultured HepG2 cells (P<0.05). The levels of caspase3 mRNA and protein were significantly upregulated in mIBEC cocultured HepG2 cells compared with HepG2 cells cultured alone (P<0.05). ConclusionmIBEC can inhibit the proliferation of cocultured HepG2, and caspase3 activation might be one of the reasons for the inhibitory effect of mIBEC against HepG2 cells.
Key words:  liver neoplasms  biliary epithelial cells  HepG2 cells  co-culture  caspase3  apoptosis