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Wnt/β-catenin通路与KLF4在胃肠道肿瘤中的作用及其机制 被引量：4

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摘要 β-catenin作为Wnt通路的核心蛋白,调节Wnt相关基因的表达并参与细胞增殖的调控和转录,介导同型细胞间的黏附从而抑制肿瘤的浸润和转移。β-catenin基因突变或功能异常可导致其功能激活和在核内聚积,调节肿瘤发生发展、弥散甚至转移。转录因子KLF4主要在分化期的胃肠道上皮等细胞内高表达,主要生理功能为调节细胞增殖与分化。KLF4在多种胃肠道肿瘤中表达降低,且敲除胃肠道上皮KLF4后,胃肠道上皮呈增殖及分化改变,这表明KLF4是维持胃肠道上皮稳态的关键因素之一。笔者对β-catenin与KLF4相互作用对胃肠道肿瘤生物行为影响的研究进行综述。
作者 张能 王子卫
机构地区 重庆医科大学附属第一医院胃肠外科
出处 《中国普通外科杂志》 CAS CSCD 北大核心 2011年第10期1109-1112,共4页 China Journal of General Surgery
基金 重庆市卫生局医学科学技术研究重点项目(2010-1-19)
关键词 胃肠肿瘤 WNT/Β-CATENIN Krüppel样因子4(KLF4) 综述文献
分类号 R735.23 [医药卫生—肿瘤]
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参考文献27

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二级参考文献35

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共引文献16

同被引文献31

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二级引证文献14

中国普通外科杂志
2011年 第10期

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