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c-Myc在Apc突变体肠道表型中的作用:结案还是新起点的时候了?

Role of c-Myc in Apc mutant intestinal phenotype: case closed or time for a new beginning?

作者信息

Bommer Guido T, Fearon Eric R

机构信息

Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.

出版信息

Cancer Cell. 2007 May;11(5):391-4. doi: 10.1016/j.ccr.2007.04.015.

Abstract

Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene occurs in most colorectal cancers. The proto-oncogene c-MYC was one of the first genes linked to APC inactivation, but the in vivo significance of c-MYC's enhanced expression in intestinal cells with APC defects has been uncertain. Sansom et al. recently reported that targeted inactivation of c-Myc in murine intestinal epithelium potently inhibited phenotypical and transcriptional changes seen in Apc-deficient intestinal epithelium. While these findings are very interesting, some questions remain about the assignment of c-Myc as the pre-eminent beta-catenin-regulated gene in intestinal epithelium.

摘要

大多数结直肠癌中都会发生腺瘤性息肉病 coli(APC)肿瘤抑制基因的失活。原癌基因 c-MYC 是最早与 APC 失活相关的基因之一,但 c-MYC 在具有 APC 缺陷的肠道细胞中表达增强的体内意义尚不确定。桑索姆等人最近报告称,在小鼠肠道上皮中靶向失活 c-Myc 可有效抑制 Apc 缺陷型肠道上皮中出现的表型和转录变化。虽然这些发现非常有趣,但关于将 c-Myc 认定为肠道上皮中主要的 β-连环蛋白调节基因仍存在一些问题。

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