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作 者:黄清玲[1] 薛会丽[1] 郑大利[1] 林建银[1]
机构地区:[1]福建医科大学分子医学研究中心,福州市350004
出 处:《医学分子生物学杂志》2007年第6期489-493,共5页Journal of Medical Molecular Biology
基 金:福建省自然科学基金(No.C0410015);福建省科技厅资助项目(No.2005D101)~~
摘 要:目的研究分析67ku层黏连蛋白受体(laminin receptor,67LR)与肝癌细胞基质金属蛋白酶(matrix metalloproteinases,MMPs)及其组织抑制因子(tissue inhibitor of metalloproteinases,TIMPs)表达的关系,探讨67LR促进肝癌细胞体外侵袭能力的分子机制。方法以67LR转染HepG2的稳定细胞株及其对照细胞为材料,采用半定量RT-PCR分析目前已知的23种MMPs和4种TIMPs的表达及变化情况,对表达有变化的基因采用荧光定量PCR进行验证,采用明胶酶谱分析MMP活性的变化。结果半定量RT-PCR和荧光定量PCR发现,67LR高表达的LR4细胞,其MMP2,9的表达比67LR低表达的LR6及对照组pcD-NA-1细胞明显升高,明胶酶谱分析也揭示,LR4细胞分泌的MMP-2和MMP-9的活性明显上升。结论67LR可以促进肝癌细胞MMP-2和MMP-9的表达和分泌,从而促进肝癌细胞体外侵袭能力。Objective The aim of this proteinases (MMPs) and tissue inhibitors of study was to examine the expression of matrix metallo- metalloproteinases (TIMPs) and to explore the molecular mechanism of 67LR-enhanced invasion of HepG2 cells. Methods Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of 23 kinds of MMPs and 4 kinds of TIMPs in HepG2 pcDNA-1. Quantitative real-time PCR and gelatin zymography were conducted to confirm the results of semi-quantitative RT-PCR. Results In the LR4 cells with high 67LR expressions, the expressions of MMP-2, MMP-9 were significantly higher that those in LR6 cells with lower 67LR expression and pcDNA-1 cells serving as control. Zymography showed that the activity of MMP-2 and MMP-9 secreted by LR4 was significantly increased. Conclusion The 67LR can promote the expression and secretion of MPP-2 and MMP-9 in hepatocellular carcino- ma cells in vitro thereby increasing the invasion of hepatocellular carcinoma ceils.
关 键 词:肝癌细胞 层黏连蛋白受体 基质金属蛋白酶 组织金属蛋白酶抑制剂
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