Kantor J D, McCormick B, Steeg P S, Zetter B R
Department of Physiology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Cancer Res. 1993 May 1;53(9):1971-3.
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.
摘要 在某些肿瘤（包括黑色素瘤、乳腺癌和肝细胞癌）中，nm23基因表达与肿瘤转移潜能呈负相关。nm23蛋白直接或间接调节转移表型的细胞机制尚不清楚。由于细胞运动在转移扩散中起着至关重要的作用，我们研究了用nm23互补DNA转染的肿瘤细胞在迁移能力上是否有任何改变。我们的结果表明，nm23转染抑制了小鼠黑色素瘤细胞和人乳腺癌细胞对血清或特定因子（如血小板衍生生长因子或胰岛素样生长因子1）的迁移反应能力。在nm23转染细胞中，随机的、未受刺激的细胞运动并未受到抑制。结果表明，在两种不同的肿瘤细胞系统中，nm23基因产物可能与刺激细胞运动所必需的细胞内分子相互作用。
