Adiponectin suppresses tumorigenesis in ApcMin/+ mice
Adiponectin suppresses tumorigenesis in ApcMin/+ mice
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DOI：
10.1016/j.canlet.2009.06.037
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发表时间：
2010-02-28
期刊：
影响因子：
9.7
通讯作者：
Nagawa, Hirokazu
中科院分区：
文献类型：
--
作者：
Otani, Kensuke;Kitayama, Joji;Nagawa, Hirokazu
最近的研究表明，脂联素对多种恶性肿瘤具有抑制作用。为了阐明脂联素在结直肠癌发生中的作用，我们研究了外源性脂联素对具有Apc基因点突变的C57 BL/6 J-Apc（Min/+）小鼠肠息肉形成的影响。我们发现脂联素治疗显著减少了小肠腺瘤性息肉的数量，特别是直径大于2 mm的息肉。脂联素的两种主要受体AdipoR 1和AdipoR 2在腺瘤性息肉中表达，注射脂联素不会改变其表达水平。总之，脂联素抑制Apc（Min/+）小鼠肠腺瘤的生长。提高脂联素水平可能是在大肠癌发生早期预防大肠癌的新策略。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
Recent reports have shown that adiponectin has a suppressive effect on various types of malignancy. In order to clarify the role of adiponectin in colorectal carcinogenesis, we examined the effect of exogenous administration of adiponectin on intestinal polyp formation in C57BL/6J-Apc(Min/+) mice, which possess a point mutation in the Apc gene. And we found that adiponectin treatment significantly decreased the number of adenomatous polyps, especially polyps larger than 2 mm in diameter, in the small intestine. Two major receptors for adiponectin, AdipoR1 and AdipoR2, were expressed in adenomatous polyps, and their expression levels were not altered by adiponectin injection. in conclusion, adiponectin suppresses the growth of intestinal adenomas in the Apc(Min/+) mice. Increasing the adiponectin level may be a new strategy for the prevention of colorectal cancer at an early step of carcinogenesis. (C) 2009 Elsevier Ireland Ltd. All rights reserved.