染色质解旋酶/ATP酶的DNA结合蛋白1样基因致瘤机制研究进展  

A Review of CHD1L Tumorigenic Mechanism

作　　者：傅点[1] 王玲[1] 田丰[1] 程文[1] 

机构地区：[1]南京军区南京总医院泌尿外科,南京210002

出　　处：《医学综述》2015年第14期2562-2565,共4页Medical Recapitulate

摘　　要：染色质解旋酶/ATP酶的DNA结合蛋白1样基因(CHD1L)是一种新近被证实与在许多实体瘤中表达增多的致癌基因,它定位于第1号染色体q21区。CHD1L在肝细胞癌和其他肿瘤中的功能性研究提示,该基因在肿瘤形成过程中可以引起细胞增殖、调节G1/S过渡期并且可以抑制细胞凋亡。CHD1L活化的潜在机制可能是通过结合凋亡蛋白Nur77,或通过上调CHD1L调控的靶基因(如ARHGEF9、SPOCK1或TCTP)受体以激活蛋白激酶B通路,从而干扰细胞死亡程序。CHD1L目前已经被认为是一种新的可独立评价一些实体性肿瘤进展、预后以及生存率的生物标志物。现有的对CHD1L的认识在将来也许可以激励大家进行对一些特定肿瘤的靶向治疗研究。Chromodomain helicase/ATPase DNA binding protein 1-like （CHD1L） gene is a newly iden-tified oncogene located at 1q21 amplification in many solid tumors.The functional studies of CHD1L in hepa-tocellular carcinoma and other tumors strongly suggested its oncogenic role in tumoregenesis for unleashed cell proliferation,G1/S transition and inhibition of apoptosis.The underlying mechanisms of CHD1L activation may disrupt the cell death program via binding apoptotic protein Nur77 or through activation of AKT pathway by up-regulation of CHD1L-mediated target genes（such as ARHGEF9,SPOCK1 or TCTP）.CHD1L is now considered to be a novel independent biomarker for progression , prognosis and survival in several solid tumors.The accumulated knowledge of CHD1L will invigorate the search for targeted treatment in specific subtype of tumors in the future.

关 键 词：染色质解旋酶/ATP酶的DNA结合蛋白1样基因 致癌基因 染色体1q21 扩增 ρ鸟嘌呤核苷酸交换因子9 蛋白聚糖1 Nur77 

分 类 号：R34[医药卫生—基础医学]