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Id2在小鼠家族性腺瘤性息肉病发生中的作用

Department of General Surgery,Shenyang Weikang Hospital, Shengyang110021, China

  • 摘要: 研究DNA结合抑制物2(inhibitor of DNA binding2, Id2) 在 ApcΔ716/+小鼠家族性腺瘤性息肉病(familial adenomatous polyposis,FAP)发生中的作用。方法 Id2基因缺失的基因工程小鼠和家族性腺瘤性息肉病模型ApcΔ716/+小鼠杂交后,统计ApcΔ716/+小鼠与ApcΔ716/+Id2-/-杂交小鼠小肠肠道息肉的数目及总负荷,通过Western blot及原位杂交技术测定腺瘤性息肉Id2的表达。结果 腺瘤性息肉组织中Id2 蛋白及mRNA表达明显升高,相比ApcΔ716/+Id2野生型小鼠,ApcΔ716/+Id2-/-杂交小鼠肠道息肉总数目与不同大小的肠道息肉数目有明显减少(P均<0.05)。结论 肠道腺瘤性息肉组织中Id2表达升高,Id2的缺失能抑制ApcΔ716/+小鼠肠道腺瘤性息肉的发生,Id2在人类家族性腺瘤性息肉病中可能发挥着促进肠道息肉形成的作用。

     

    Abstract: Objective To investigate the role of Id2 in the development and growth of familial adenomatous polyposis in ApcΔ716/+ mice. Methods ApcΔ716/+ mice were hybridized with Id2 defi cient mice, and the tumor susceptibility in intestine was compared. The total intestine polyps number and overall load of ApcΔ716/+Id2+/+mice and ApcΔ716/+Id2-/- mice were analyzed and the changes in intestinal polyps were observed. The western blot and in situ hybridization were performed to investigate the expression of Id2 in intestinal polyps. Result The protein and mRNA expression of Id2 was increased in the intestinal polyps of ApcΔ716/+ mice. Id2 defi cient in ApcΔ716/+ mice resulted in signifi cant decrease of total polyps number and polyp numbers of with different size in the intestine at 8 weeks (P all <0.05). Conclusion Id2 expression is increased in the polyps.Id2 deficiency could inhibit intestinal adenomatous polyps of APCΔ716/+ mice. Importantly, these studies also suggest that Id2 may act as a polyp promotor for human familial adenomatous polyposis.

     

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