LINC00908 attenuates LUAD tumorigenesis through DEAD-box helicase 54

被引:1
作者
Zhao, Jiahua [1 ,2 ]
Yang, Xuhui [2 ,3 ]
Gong, Wenwen [4 ]
Zhang, Lin [5 ]
Li, Chenxi [2 ,3 ]
Han, Xiao [2 ,3 ]
Zhang, Yang [6 ]
Chu, Xiangyang [2 ,7 ]
机构
[1] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 6, Dept Thorac Surg, Beijing, Peoples R China
[2] Chinese PLA Med Sch, Beijing, Peoples R China
[3] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 5, Dept Oncol, Beijing, Peoples R China
[4] Med Supplies Ctr PLA Gen Hosp, Dept Pharm, Beijing, Peoples R China
[5] Air Force Med Univ, Hosp 986, Dept Outpatient Serv, Xian, Shaanxi, Peoples R China
[6] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 2, Dept Cardiol, Beijing, Peoples R China
[7] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 1, Dept Thorac Surg, Beijing, Peoples R China
关键词
Lung adenocarcinoma; LINC00908; DDX54; RFX2; glycolysis; CANCER; GLYCOLYSIS; METABOLISM; RNA;
D O I
10.62347/HXZM6394
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Lung adenocarcinoma (LUAD) is one of the leading causes of cancer -related death worldwide. We identified a specific long non -coding RNA (LncRNA), LINC00908, which was downregulated in LUAD tissues and associated with good outcome. LINC00908 inhibited glycolysis by regulating the expression of the DEAD -box helicase 54 (DDX54), which was screened by a nine -gene risk signature, where DDX54 showed a positive correlation with several glycolysis-related genes. Experimental verification confirmed that DDX54 regulated nine key glycolytic enzymes, thereby affecting the level of glycolysis in LUAD. Further, the expression of LINC00908 in LUAD tumorigenesis was modulated by a transcription factor, regulatory factor X2 (RFX2). The RFX2/LINC00908/DDX54 axis regulated LUAD tumor growth, migration, invasion, cell apoptosis and glycolysis both in vitro and in vivo . These results demonstrate that this axis may serve as a novel mediator in LUAD progress and offer a novel therapeutic target for more precise diagnosis and treatment of LUAD.
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页数:29
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