缺乏功能性结直肠癌缺失基因（Dcc）的小鼠的表型。

Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene.

作者信息

Fazeli A, Dickinson S L, Hermiston M L, Tighe R V, Steen R G, Small C G, Stoeckli E T, Keino-Masu K, Masu M, Rayburn H, Simons J, Bronson R T, Gordon J I, Tessier-Lavigne M, Weinberg R A

机构信息

Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Cambridge 02142, USA.

出版信息

Nature. 1997 Apr 24;386(6627):796-804. doi: 10.1038/386796a0.

DOI:10.1038/386796a0

PMID:9126737

Abstract

The DCC (Deleted in colorectal cancer) gene was first identified as a candidate for a tumour-suppressor gene on human chromosome 18q. More recently, in vitro studies in rodents have provided evidence that DCC might function as a receptor for the axonal chemoattractant netrin-1. Inactivation of the murine Dcc gene caused defects in axonal projections that are similar to those observed in netrin-1-deficient mice but did not affect growth, differentiation, morphogenesis or tumorigenesis in mouse intestine. These observations fail to support a tumour-suppressor function for Dcc, but are consistent with the hypothesis that DCC is a component of a receptor for netrin-1.

摘要

结直肠癌缺失基因（DCC）最初被确定为人类18号染色体上肿瘤抑制基因的候选基因。最近，对啮齿动物的体外研究表明，DCC可能作为轴突化学引诱剂netrin-1的受体发挥作用。小鼠Dcc基因的失活导致轴突投射缺陷，这与在netrin-1缺陷小鼠中观察到的缺陷相似，但不影响小鼠肠道的生长、分化、形态发生或肿瘤发生。这些观察结果不支持Dcc具有肿瘤抑制功能，但与DCC是netrin-1受体组成部分的假说一致。