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Evi-1基因的生物学作用及致肿瘤机制研究进展 被引量:1

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摘要 逆转录病毒结合位点-1(Evi-1)基因是首先在小鼠粒细胞白血病发现的逆转录病毒结合位点。在恶性血液系统病变及其他实体肿瘤中高表达,致肿瘤机制主要为通过抑制Smads而抑制转化生长因子-β(TGF-β)信号途径,调节细胞周期,促进血管生成,抑制C-Jun氮末端激酶(JNK)及激活转录因子激活蛋白-1(AP-1)等。 Ecotropic viral integration site-1 (Evi-1) gene is first identified as a binding site for retrovirus in murine myeloid leukemia.The human homologue with the murine in leukemia oncogene Evi-1 is about 91% of nuclear sequence and 94% of amino acid.Evi-1 gene is high expressed in myeloid malignancies and other tumors.The main tumorigenic mechanisms of Evi-1 gene include inhibiting TGF-β signal path by depressing Smad3,adjusting cell cycle,promoting angiogenesis,inhibiting JNK.activating AP-1,and so on.
作者 丁向萍
出处 《国际肿瘤学杂志》 CAS 2013年第3期170-173,共4页 Journal of International Oncology
基金 甘肃卫生行业科研计划项目
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