Bommer Guido T, Fearon Eric R
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.
Cancer Cell. 2007 May;11(5):391-4. doi: 10.1016/j.ccr.2007.04.015.
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.
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。
