SALL4基因在肝内胆管癌中通过抑制KLF4基因表达促进EMT改变  被引量:3

SALL4 Promotes EMT in Intrahepatic Cholangiocarcinoma by Inhibiting KLF4 Expression

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作  者:邓刚[1] 蔡谭兴 雷钊[1] 汤凡凡 徐宏博[1] 黄飞舟[1] 上官丹罡[2] 陈小娟 DENG Gang;CAI Tanxing;LEI Zhao;TANG Fanfan;XU Hongbo;HUANG Feizhou;SHANGGUAN Dangang;CHEN Xiaojuan(Department of Hepatobiliary and Pancreatic Surgery,the Third Xiangya Hospital of Central South University,Changsha,Hunan,410013,China;Pharmacy Department,Hunan Cancer Hospital,Changsha,Hunan,410013,China)

机构地区:[1]中南大学湘雅三医院肝胆胰外科,湖南长沙410013 [2]湖南省肿瘤医院药学部,湖南长沙410013

出  处:《肿瘤药学》2021年第1期36-39,共4页Anti-Tumor Pharmacy

基  金:湖南省自然科学基金项目(2017JJ2336);长株潭国家自主创新示范区专项(2017XK2108)。

摘  要:目的探究SALL4基因与KLF基因在肝内胆管癌中的相互作用与影响。方法采用生物信息学方法预测SALL4与KLF4基因启动子之间的作用位点,并通过荧光素酶报告系统进行验证;RNA干扰技术对SALL4基因进行敲除,Western blotting检测KLF4蛋白的表达;免疫组化法检测临床样本中SALL4与KLF4蛋白的表达,并结合TCGA数据库进行验证。结果KLF4启动子上存在SALL4结合的模序,且二者的表达呈负相关。结论在肝内胆管癌中,SALL4能够结合KLF4启动子区域,抑制KLF4基因的表达。在肝内胆管癌细胞株中敲低SALL4基因,可使E-cadherin表达显著提高,提示SALL4能够促进上皮间质转化(EMT)的改变。Objective To explore the interaction and effects of SALL4 gene and KLF gene in intrahepatic cholangiocarcinoma.Methods The interaction site between SALL4 and KLF4 gene promoter was predicted by bioinformatics method and verified by luciferase reporter system.SALL4 gene was knocked out by RNA interference,and KLF4 protein expression was detected by Western blotting.The expression of SALL4 and KLF4 proteins in clinical samples was detected by immunohistochemistry,and verified by TCGA database.Results There were SALL4 binding motifs on the KLF4 promoter.And there was a negative correlation between the expressions of SALL4 and KLF4 in vivo and in vitro.Conclusion SALL4 can bind to KLF4 promoter region and inhibit KLF4 gene expression in intrahepatic cholangiocarcinoma.Knockdown of SALL4 increased the expression of E-cadherin,suggesting that SALL4 could promote epithelial-mesenchymal transition.

关 键 词:SALL4 KLF4 肝内胆管癌 上皮间质转化 

分 类 号:R735.8[医药卫生—肿瘤]

 

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