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Igf2印记缺失会改变小鼠肠道成熟和肿瘤发生。

Loss of imprinting of Igf2 alters intestinal maturation and tumorigenesis in mice.

作者信息

Sakatani Takashi, Kaneda Atsushi, Iacobuzio-Donahue Christine A, Carter Mark G, de Boom Witzel Sten, Okano Hideyuki, Ko Minoru S H, Ohlsson Rolf, Longo Dan L, Feinberg Andrew P

机构信息

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

出版信息

Science. 2005 Mar 25;307(5717):1976-8. doi: 10.1126/science.1108080. Epub 2005 Feb 24.

Abstract

Loss of imprinting (LOI) of the insulin-like growth factor II gene (IGF2) is an epigenetic alteration that results in a modest increase in IGF2 expression, and it is present in the normal colonic mucosa of about 30% of patients with colorectal cancer. To investigate its role in intestinal tumorigenesis, we created a mouse model of Igf2 LOI by crossing female H19+/- mice with male Apc+/Min mice. Mice with LOI developed twice as many intestinal tumors as did control littermates. Notably, these mice also showed a shift toward a less differentiated normal intestinal epithelium, reflected by an increase in crypt length and increased staining with progenitor cell markers. A similar shift in differentiation was seen in the normal colonic mucosa of humans with LOI. Thus, altered maturation of nonneoplastic tissue may be one mechanism by which epigenetic changes affect cancer risk.

摘要

胰岛素样生长因子II基因(IGF2)印记缺失(LOI)是一种表观遗传改变,会导致IGF2表达适度增加,约30%的结直肠癌患者的正常结肠黏膜中存在这种情况。为了研究其在肠道肿瘤发生中的作用,我们通过将雌性H19+/-小鼠与雄性Apc+/Min小鼠杂交,创建了一个Igf2 LOI小鼠模型。具有LOI的小鼠发生的肠道肿瘤数量是对照同窝小鼠的两倍。值得注意的是,这些小鼠还表现出向分化程度较低的正常肠上皮转变,表现为隐窝长度增加和祖细胞标志物染色增加。在具有LOI的人类正常结肠黏膜中也观察到了类似的分化转变。因此,非肿瘤组织成熟的改变可能是表观遗传变化影响癌症风险的一种机制。

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