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目的 研究胰岛素样生长因子 型受体 (IGF- R)对肝细胞癌生物学行为的影响。 方法 应用免疫组化 SP法检测肝细胞癌、癌旁和正常肝组织 IGF- R的表达。构建 IGF- R正、反义基因真核表达载体 ,经脂质体介导转入 SMMC- 772 1肝癌细胞株 ,观测 IGF- R正、反义基因对肝癌细胞生物学行为的影响。 结果 (1)在肝癌组织中 IGF- R呈过度表达(90 .3% ) ,以膜、胞浆混合型表达为主 ,显著高于正常肝组织。肝癌多发结节组高于单发结节组 (P<0 .0 5 )。 (2 ) IGF- R反义基因能明显下调内源性 IGF- R的表达 ,与 772 1细胞、正义细胞有显著性差异 (P<0 .0 1)。 (3)电镜下反义细胞内可见微腺腔、灶性坏死、髓鞘样结构。 4反义细胞 G0 /G1期明显增加 (6 3.9% ) ,S期减少 (19.3% ) ,细胞凋亡增加 (5 .89% ) ,与 772 1细胞、正义细胞有显著性差异 (P<0 .0 1)。 5 .反义细胞不能在软琼脂中生长。 结论 (1) IGF- R高表达与肝癌的发生及侵袭性行为有密切关系。 (2 ) IGF- R反义基因下调 772 1细胞内源性 IGF- R的表达 ,对肝癌细胞的增殖有明显抑制作用。
Objective To study the effect of insulin-like growth factor receptor (IGF-R) on the biological behavior of hepatocellular carcinoma. Methods Immunohistochemical SP method was used to detect the expression of IGF-R in hepatocellular carcinoma, paracancer and normal liver tissues. The eukaryotic expression vectors of sense and antisense IGF-R gene were constructed and transfected into SMMC-772 1 hepatocellular carcinoma cell line by liposome. The effect of positive and negative sense and antisense IGF-R gene on the biological behavior of hepatocellular carcinoma cell was observed. Results (1) IGF-R was overexpressed in hepatocellular carcinoma (90.3%), mainly in mixed membrane and cytoplasm, and significantly higher than that in normal liver tissue. Multiple nodules of hepatocellular carcinoma were higher than single nodules (P <0.05). (2) The IGF-R antisense gene could significantly downregulate the expression of endogenous IGF-R, which was significantly different from that of 772 1 cells and normal cells (P <0.01). (3) Micro-gland cavity, focal necrosis and myelin-like structure were observed in antisense cells under electron microscope. 4 antisense cells increased significantly in G0 / G1 phase (6 3.9%), decreased in S phase (19.3%), increased apoptosis (5.89%), significantly different from that in 772 1 cells .0 1). Antisense cells can not grow on soft agar. Conclusion (1) The high expression of IGF-R is closely related to the occurrence and aggressive behavior of HCC. (2) The IGF-R antisense gene down-regulated the expression of endogenous IGF-R in 772 1 cells, which significantly inhibited the proliferation of hepatoma cells.