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多磷酸肌醇-5-磷酸酶Ⅱ通过影响 Akt 表达调控结直肠癌增殖和侵袭

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摘要 多磷酸肌醇-5-磷酸酶Ⅱ(inositol polyphosphate 5-phosphataseⅡ,SHIP2)是多磷酸肌醇-5-磷酸酶家族的一员,人类 SHIP2由位于染色体11q23上的 INPP 5L1基因编码, mRNA 长度为4737 bp[1]。研究表明,SHIP2在调节胰岛素信号通路促进糖尿病和肿瘤的发生,以及细胞骨架蛋白的重塑,细胞的黏附和受体介导的内吞等方面具有重要作用。SHIP2通过水解磷脂酰肌醇-3-羟激酶(phosphatidylinositol 3-hydroxy kinase,PI3K),促使 PI3K 转变为磷脂酰肌醇2-激酶(phosphatidylinositol 2-hydroxy kinase,PI2K),抑制 Akt的活化,负性调节 PI3K/Akt 信号通路而抑制肿瘤的发生[2]。但也有研究表明,SHIP2促进某些肿瘤的发生、发展。Prasad 等[3]在体内和体外实验中证明,高表达 SHIP2能促进乳腺癌细胞增长与远处转移。另有文献报道,SHIP2可以促进前列腺癌和喉癌的发生[4]。本研究主要探讨 SHIP2在结直肠癌标本中的表达情况,以及对结直肠癌细胞系增殖和侵袭的影响。
出处 《中华消化杂志》 CAS CSCD 北大核心 2016年第1期49-52,共4页 Chinese Journal of Digestion
基金 上海市科学技术委员会基金(13DZ1942806)
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