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目的 探讨nm2 3 H1 基因转染靶向阻断人高转移大细胞肺癌细胞株L9981Wnt信号传导通路的可行性 ,为阐明nm2 3 H1 基因调控肺癌转移抑制的分子机制和靶向治疗提供实验依据。方法 以转染nm 2 3 H1 基因的L9981 nm 2 3 H1 、原代L9981、空载L9981 pLXSN三株人高转移大细胞肺癌细胞为研究对象 ,应用Westernblot检测比较各株肺癌细胞胞浆、胞核中Wnt信号传导通路关键激酶GSK 3 β和 β 连环蛋白表达的变化。结果 ①GSK 3 β在L9981 nm 2 3 H1 肺癌细胞胞浆中表达量IOD( 63 41± 5 41)显著高于L9981( 373 6± 2 98)和L9981 pLXSN( 3 613± 3 83 ) (P <0 .0 0 1) ;②GSK 3 β在L9981 nm2 3 H1 肺癌细胞胞核中表达量IOD( 4 3 5 6± 490 )显著高于L9981( 65 7± 5 7)和L9981 pLXSN ( 70 5± 75 ) (P <0 .0 0 1) ;③β 连环蛋白在L9981 nm 2 3 H1 肺癌细胞胞浆中表达量IOD( 3 64 9± 118)显著高于L9981( 14 0 1± 3 1)和L9981 pLXSN ( 13 5 0± 5 5 )(P <0 .0 0 1) ;④β 连环蛋白在L9981 nm 2 3 H1 肺癌细胞胞核中表达量IOD( 2 945± 68)与L9981( 2 60 4± 2 3 )和L9981 pLXSN( 2 65 2± 5 3 )比较无显著性差异 (P >0 .0 5 ) ;⑤L9981与L9981 pLXSN两者间GSK 3 β和β 连环蛋白在肺癌细胞胞浆和胞核的?
Objective To investigate the feasibility of targeting nm23 H1 gene transfection to block the L9981 Wnt signal transduction pathway in human high metastatic large cell lung cancer cell line LNCS and to provide experimental evidence for elucidating the molecular mechanism and targeting therapy of nm23 H1 gene regulating lung metastasis. Methods L9981 nm 2 3 H1 transfected with nm 2 3 H1 gene, primary L9981 and L9981 pLXSN were transfected into three human highly metastatic large cell lung cancer cells. Western blotting was used to detect the cytosolic and nuclear Changes in the Expression of Key Kinase GSK 3 β and β Catenin in Wnt Signaling Pathway. Results ① The expression level of GSK 3 β in cytoplasm of L9981 nm 2 3 H1 lung cancer cells was significantly higher than that of L9981 (373 6 ± 2 98) and L9981 pLXSNs (3613 ± 3 83) (P <0 .0 0 1). ② The expression of GSK 3 β in the nucleus of L9981 nm2 3 H1 lung cancer cells was significantly higher than that of L9981 (65 7 ± 5 7) and L9981 pLXSNs (75 ± 75) (P <0.01). ③ The expression level of β-catenin in cytoplasm of L9981 nm 2 3 H1 lung cancer cells was significantly higher than that of L9981 (14 0 1 ± 3 1) and L9981 pLXSN The expression of β-catenin in nuclei of L9981 nm 2 3 H1 lung cancer cells was significantly higher than that of L9981 (2 60 ± 3 3) There was no significant difference between L9981 and pLXSN (2 652 ± 5 3) (P> 0.05). (5) The expressions of GSK 3 β and β-catenin in L9981 and L9981 pLXSN in the cytoplasm and nucleus of lung cancer cells