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目的 探讨nm2 3 H1转染和蛋白激酶C(PKC)特异抑制剂CalphostinC对人高转移大细胞肺癌细胞株L9981细胞PKC信号转导通路的作用 ,以及nm2 3 H1基因对PKC激活转位的影响。方法 应用激光扫描共聚焦显微镜观察nm 2 3 H1基因转染前后和CalphostinC处理转基因细胞株L9981 nm2 3 H1前后PKC在不同的亚细胞区域的定位情况。结果 ( 1)原代细胞株L9981和空载体细胞株L9981 pLXSN中PKC α、PKC βⅡ主要位于胞核及核周 ,处于激活状态 ;转染nm 2 3 H1基因后的人肺癌细胞株L9981 nm2 3 H1中PKC α、PKC βⅡ主要位于胞浆 ,处于未激活状态。 ( 2 )CalphostinC作用后所有细胞中的PKC均主要位于胞浆中 ,处于未激活状态。结论 ( 1)nm2 3 H1基因可使L9981细胞株中PKC从胞核向胞浆转位 ,从而抑制PKC信号转导。 ( 2 )CalphostinC可使L9981、L9981 pLXSN细胞株中PKC从胞核向胞浆转位 ,从而抑制PKC信号转导。
Objective To investigate the effect of nm23 H1 transfection and protein kinase C (PKC) inhibitor CalphostinC on PKC signal transduction pathway in human high metastatic large cell lung cancer cell line L9981 and the effect of nm23 H1 gene on PKC activation and translocation. Methods The localization of PKC in different subcellular regions before and after the transfection of nm 2 3 H1 gene and CalphostinC-treated transgenic L9981 nm2 3 H1 cells were observed by laser scanning confocal microscopy. Results (1) PKCα and PKCβⅡ in primary cell line L9981 and empty vector L9981 pLXSN were mainly located in the nucleus and perinucleus, and were activated. The human lung cancer cell line L9981 nm2 3 transfected with nm 2 3 H1 gene H1 PKC α, PKC β Ⅱ mainly located in the cytoplasm, in an inactive state. (2) PKC in all cells after CalphostinC treatment was mainly located in the cytoplasm, and was inactive. Conclusion (1) The nm23 H1 gene translocates PKC from the nucleus to the cytoplasm in L9981 cell line and inhibits PKC signal transduction. (2) CalphostinC can inhibit the PKC signal transduction of PKC from nucleus to cytoplasm in L9981 and L9981 pLXSN cell lines.