Risk SNP-induced lncRNA-SLCCl drives colorectal cancer through activating glycolysis signaling

查看全文 作　　者：Tingting [1]Yan;Chaoqin [1]Shen;Penglei [2]Jiang;Chenyang [1]Yu;Fangfang [1]Guo;Xianglong [1]Tian;Xiaoqiang [1]Zhu;Shiyuan [1]Lu;Bingshe [2]Han;Ming [3]Zhong;Jinxian [3]Chen;Qiang [4]Liu;Yingxuan [1]Chen;Junfang [2]Zhang;Jie [1]Hong;Haoyan [1]Chen;Jing-Yuan [1]Fang

机构地区：[1]State Key Laboratory for Oncogenes and Related Genes,Key Laboratory of Gastroenterology&Hepatology,Ministry of Health,Division of Gastroenterology and Hepatology,Shanghai Cancer Institute,Shanghai Institute of Digestive Disease,Renji Hospital,Shanghai Jiao Tong University School of Medicine,145 Middle Shandong Road,200001 Shanghai,China;[2]Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,College of Fishery and Life Science,Shanghai Ocean University,Shanghai 201306,China;[3]Division of Gastrointestinal Surgery,Renji Hospital,School of Medicine,Shanghai Jiao Tong University,145 Middle Shandong Road,200001 Shanghai,China;[4]Department of Pathology,Renji Hospital,School of Medicine,Shanghai Jiao Tong University,145 Middle Shandong Road,200001 Shanghai,China

出　　处：《Signal Transduction and Targeted Therapy》索引2021年第6卷第3期,共13页

基　　金：supported in part by grants from the State Key R&D Program(2020YFA0509200);the National Natural Science Foundation of China(81421001,81530072,81830081,81871901,81874159,81902368,31970718,81770165);Shanghai Municipal Health Commission,Collaborative Innovation Cluster Project(2019CXJQ02);'Shu Guang'project supported by Shanghai Municipal Education Commission and Shanghai Education Developm ent Foundation(17SG18);the Program for Professor of Special Appointm ent(Eastern Scholar No.201268 and 2015 Youth Eastern Scholar No.QD2015003)at Shanghai Institutions of Higher Learning;Shanghai Municipal Education Commission—Gaofeng Clinical Medicine Grant Support(No.20152512,20161309);Innovative research team of high-level local universities in Shanghai. 摘　　要：Long non-coding RNAs(lncRNAs)play key roles in colorectal carcinogenesis.Here,we aimed to identify the risk SNP-induced lncRNAs and to investigate their roles in colorectal carcinogenesis.First,we identified rs6695584 as the causative SNP in 1 q41 locus.The A>G mutation of rs6695584 created a protein-binding motif of BATF,altered the enhancer activity,and subsequently activated IncSLCCl expression.Further validation in two independent CRC cohorts confirmed the upregulation of IncSLCCl in CRC tissues,and revealed that increased IncSLCCl expression was associated with poor survival in CRC patients.Mechanistically,lncRNA-SLCCl interacted with AHR and transcriptionally activated HK2 expression,the crucial enzyme in glucose metabolism,thereby driving the glycolysis pathway and accelerating CRC tumor growth.The functional assays revealed that IncSLCCl induced glycolysis activation and tumor growth in CRC mediated by HK2.In addition,HK2 was upregulated in colorectal cancer tissues and positively correlated with IncSLCCl expression and patient survival.Taken together,our findings reveal a risk SNP-mediated oncogene lncRNA-SLCCl promotes CRC through activating the glycolysis pathway. 关键词：COLORECTAL GLYCOLYSIS METABOLISM

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Risk SNP-induced lncRNA-SLCCl drives colorectal cancer through activating glycolysis signaling

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