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14-3-3 蛋白诱导对 A549 人肺腺癌细胞增殖的影响。

Effect of 14-3-3 protein induction on cell proliferation of A549 human lung adenocarcinoma.

机构信息

Graduate School of Genetic Resources Technology, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan,

出版信息

Cytotechnology. 2000 Jul;33(1-3):253-7. doi: 10.1023/A:1008129020728.

Abstract

We have previously shown that 14-3-3 protein, amultifunctional adaptor molecule involved in many aspects ofsignal transduction pathways, is a target antigen for thecancer-associated human monoclonal antibody. Although recentevidences suggest a crucial role of 14-3-3 family members inthe control of cell growth and differentiation, their actualcontribution toward tumor development is still controversial. Inthis article, we examined the effect of enforced 14-3-3overexpression on cell growth of the human lung adenocarcinomacell line, A549. To address this issue, we obtained14-3-3 protein-inducible A549 sublines by transfection with14-3-3 expression vector under the control ofdexamethasone-inducible promoter. We found that 14-3-3 proteininduction in some of these sublines promoted their cell proliferation. Microscopic observation revealed that morphologyof these cells became aggressive multilayer condition,suggesting that malignant phenotypes are also acquired uponectopic induction of 14-3-3 protein.

摘要

我们之前已经表明,参与信号转导通路多方面的多功能衔接分子 14-3-3 蛋白是癌症相关的人源单克隆抗体的靶抗原。尽管最近的证据表明 14-3-3 家族成员在控制细胞生长和分化方面起着至关重要的作用,但它们对肿瘤发展的实际贡献仍存在争议。在本文中,我们研究了强制过表达 14-3-3 对人肺腺癌细胞系 A549 细胞生长的影响。为了解决这个问题,我们通过用糖皮质激素诱导启动子控制的 14-3-3 表达载体转染获得了 14-3-3 蛋白诱导的 A549 亚系。我们发现,这些亚系中的一些亚系中 14-3-3 蛋白的诱导促进了它们的细胞增殖。显微镜观察显示,这些细胞的形态变得具有侵略性的多层条件,这表明在异位诱导 14-3-3 蛋白后也获得了恶性表型。

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