增强P18^(INK4C)表达对胃腺癌细胞侵袭的影响(英文)  

Overexpressing P18 ^(INK4C) Restrains the Invasion of Gastric Adenocarcinoma Cell Line in vitro

作　　者：王楚[1] 李锋[1] 王建华[1] 应磊[1] 卢健[1] 

机构地区：[1]上海第二医科大学生物化学与分子生物学教研室,人类基因治疗研究中心上海200025

出　　处：《中国生物化学与分子生物学报》2004年第1期13-19,共7页Chinese Journal of Biochemistry and Molecular Biology

摘　　要：在应用基因芯片技术筛选胃腺癌转移相关基因的过程中 ,发现CDK抑制因子P18INK4C在人类胃腺癌转移细胞株RF 4 8中的表达较其原发灶细胞株RF 1明显下调 .这提示P18INK4C表达差异与胃腺癌细胞的侵袭转移可能有一定程度的相关性 .通过构建P18INK4C 表达质粒并将其转染入RF 4 8增强P18INK4C的表达 ,研究其对胃腺癌原发灶细胞体外运动、侵袭转移能力以及生长特性的影响 ,进一步明确P18INK4C与人类胃腺癌侵袭转移之间的关系 .结果发现 ,增强P18INK4C表达可以使胃腺癌原发灶细胞的体外侵袭能力明显下降 ,而对RF 4 8的细胞周期和生长增殖能并力未产生影响 .上述结果提示 ,P18INK4C参与人类胃腺癌转移过程 ,在此过程中其主要的作用可能并不是调节细胞周期 ,而是与胃腺癌原发灶细胞侵袭转移能力的调节密切相关 .The expression of P18 INK4C, a member of CKI, was down-regulated in RF-48, the metastatic cell line of a gastric adenocarcinoma patient, compared to RF-1, the primary cancer cell line of the same person, which was found by cDNA Microarray. Previous research indicated that inhibited expression of P18 INK4C could enhance the invasion of RF-1 in vitro. These findings implied that P18 INK4C might be involved in cell invasion and metastatic progression of human gastric adenocarcinoma. By construcing P18 INK4C expression plasmid and transfecting it into RF-48, the effects of overexpressing P18 INK4C on cell migration, invasion and proliferation ability and cell cycle were studied. Overexpression of P18 INK4C could lead to the obvious decline of cell invasion ability of RF-48 in vitro without affecting its cell cycle distribution, cell migration and proliferation ability. The results implied that P18 INK4C might play a pivotal role in regulating cell invasion rather than regulating cell cycle and proliferation as expected in the progression of human gastric adenocarcinoma.

关 键 词：P18^INK4C 表达 胃腺癌 侵袭 转移 

分 类 号：R735.2[医药卫生—肿瘤]