中文摘要：

目的：分析肝细胞癌组织及细胞系中脂肪甘油三酯脂肪酶（adipose triglyceride lipase,ATGL）的表达水平,探讨ATGL在肝细胞癌细胞增殖、迁移和侵袭过程中的作用。方法：采用蛋白质印迹法检测57对肝细胞癌组织和相应癌旁正常肝组织,以及12种肝癌细胞系中ATGL的表达水平。将靶向ATGL基因的shRNA重组慢病毒（GV248-shATGL-1、-2和-3）及其阴性对照慢病毒（GV248-shNC）分别感染肝癌Huh7和MHCC-97L细胞系,然后采用实时荧光定量PCR和蛋白质印迹法验证ATGL基因沉默效率。采用CCK-8法和Transwell小室法分别检测ATGL基因沉默对肝癌Huh7和MHCC-97L细胞增殖、迁移和侵袭的影响。结果：57例肝细胞癌患者中,有28例（49%）肝癌组织的ATGL表达水平明显高于其相应癌旁肝组织,16例（28%）肝癌组织的ATGL表达水平低于相应癌旁肝组织,而13例（23%）无明显变化。与阴性对照组相比,沉默ATGL基因表达能够明显抑制肝癌Huh7和MHCC-97L细胞增殖（P值均〈0.05）,同时细胞迁移和侵袭能力均明显降低（P值均〈0.01）。结论：肝细胞癌组织中ATGL相对高表达,而沉默ATGL基因表达可以抑制肝细胞癌Huh7和MHCC-97L细胞的增殖、迁移和侵袭。

英文摘要：

Objective： To investigate the expression of adipose triglyceride lipase （ATGL） in hepatocellular carcinoma （HCC） tissues and cell lines, and to explore the role of ATGL in proliferation, migration and invasion of HCC cells. Methods： The expression of ATGL protein in 57 pairs of HCC tissuesand their corresponding adjacent normal liver tissues as well as 12 kinds of HCC cell lines was detected by Western blotting. The recombinant lentiviruses （GV248-shATGL-1, -2, and -3） carrying specific shRNAs targeting ATGL gene were infected into HCC cell lines Huh7 and MHCC-97L. The negative control shRNA-carried lentivirus （GV248-shNC） was used as the negative control. The efficiency of ATGI_ gene-silencing was verified by real-time fuorescent quantitative PCR and Western blotting. Furthermore, the effects of ATGI gene-silencing on proliferation, migratory and invasive abilities of HCC cells were detected by CCK-8 assay and Transwell chamber assay, respectively. Results： Compared with the corresponding adjacent normal liver tissues, the expression of ATGL protein was significantly up-regulated in 49% （28/57） and down-regulated in 28% （16/57） of HCC tissues. There was no significant difference in ATGL expression between HCC tissues and the corresponding adjacent normal liver tissues in 23% （13/57） of HCC cases. The proliferation of Huh7 and MHCC-97L cells was suppressed after ATGI. gene-silencing （both P 〈 0.05）. And the migration and invasion abilities of Huh7 and MHCC-97L cells with ATGI gene-silencing were significantly decreased as compared with those in the negative control group （all P 〈 0.01）. Conclusion： The expression of ATGL is commonly up-regulated in HCC tissues. ATGI genesilencing can suppress the proliferation, migration and invasion of HCC cells.