Protein-protein interactions: a mechanism regulating the anti-metastatic properties of Nm23-H1

被引：42

作者：

Marino, Natascia ^{[1
,2
]}

Marshall, Jean-Claude ^{[1
,2
]}

Steeg, Patricia S. ^{[2
]}

机构：

[1] NIH, Bethesda, MD 20892 USA

[2] NCI, Womens Canc Sect, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA

来源：

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY | 2011年 / 384卷 / 4-5期

关键词：

Nm23-H1; Protein interactions; Metastasis; NUCLEOSIDE DIPHOSPHATE KINASE; METASTASIS SUPPRESSOR NM23-H2; CARCINOMA-CELL-LINE; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; TUMOR-METASTASIS; ADHERENS JUNCTIONS; BREAST-CANCER; H-PRUNE; COMPLEX-FORMATION; TGF-BETA;

D O I：

10.1007/s00210-011-0646-6

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Nm23-H1, also known as NDPK-A, was the first of a class of metastasis suppressor genes to be identified. Overexpression of Nm23-H1 in metastatic cell lines (melanoma, breast carcinoma, prostate, colon, hepatocellular, and oral squamous cell carcinoma) reduced cell motility in in vitro assays and metastatic potential in xenograft models, without a significant effect on primary tumor size. The mechanism of Nm23-H1 suppression of metastasis, however, is incompletely understood. Nm23-H1 has been reported to bind proteins, including those in small G-protein complexes, transcriptional complexes, the Map kinase, the TGF-beta signaling pathways and the cytoskeleton. Evidence supporting these associations is presented together with evidence of resultant biochemical and phenotypic consequences of association. Cumulatively, the data suggest that part of the anti-metastatic function of Nm23-H1 lies in pathways that it interrupts via binding and inactivation of proteins.

引用

页码：351 / 362

页数：12

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