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Risk SNP-induced lncRNA-SLCCl drives colorectal cancer through activating glycolysis signaling 被引量:4
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作者 Tingting Yan Chaoqin Shen +14 位作者 Penglei Jiang Chenyang Yu Fangfang Guo Xianglong Tian Xiaoqiang Zhu shiyuan lu Bingshe Han Ming Zhong Jinxian Chen Qiang Liu Yingxuan Chen Junfang Zhang Jie Hong Haoyan Chen Jing-Yuan Fang 《Signal Transduction and Targeted Therapy》 SCIE CSCD 2021年第3期962-974,共13页
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... 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. 展开更多
关键词 COLORECTAL GLYCOLYSIS METABOLISM
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