Inhibition of cell motility after nm23 transfection of human and murine tumor cells.
Inhibition of cell motility after nm23 transfection of human and murine tumor cells.
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发表时间：
1993-05
期刊：
影响因子：
11.2
通讯作者：
J. Kantor;Beth A. McCormick;Patricia S. Steeg;Bruce R. Zetter
中科院分区：
文献类型：
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作者：
J. Kantor;Beth A. McCormick;Patricia S. Steeg;Bruce R. Zetter
摘要nm23基因表达与某些肿瘤的转移潜能呈负相关，包括黑色素瘤、乳腺癌和肝细胞癌。nm23蛋白直接或间接调节转移表型的细胞机制尚不清楚。由于细胞运动性在转移性播散中起着重要作用，我们研究了转染nm23互补DNA的肿瘤细胞迁移能力是否有任何改变。我们的研究结果表明，nm23转染抑制小鼠黑色素瘤和人乳腺癌细胞迁移的能力，以响应血清或定义的因子，如血小板衍生生长因子或胰岛素样生长因子1。随机的，未受刺激的细胞运动性不受抑制的nm23转染子。结果表明，nm23基因产物可能与细胞内分子相互作用，这些分子在两种不同的肿瘤细胞系统中对刺激细胞运动至关重要。
Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not yet known. Because cell motility plays an essential role in metastatic dissemination, we have studied whether tumor cells transfected with nm23 complementary DNA have any alterations in their ability to migrate. Our results demonstrate that nm23 transfection inhibits the ability of murine melanoma and human breast carcinoma cells to migrate in response to serum or to defined factors such as platelet derived growth factor or insulin-like growth factor 1. Random, unstimulated cell motility was not depressed in the nm23 transfectants. The results suggest that the nm23 gene product may interact with intracellular molecules that are essential for stimulated cell motility in two different tumor cell systems.