LINC00908 promotes malignant progression and glycolysis in lung adenocarcinoma via interactions with DDX54 and RFX2

Abstract

Abstract Lung adenocarcinoma (LUAD) is one of the leading causes of cancer-related death worldwide. We identified a specific LncRNA, LINC00908, was downregulated in LUAD tissues and associated with good outcome. LINC00908 inhibited glycolysis by regulating the expression of the DEAD-box54 (DDX54), which was screened by a nine-gene risk signature related to glycolysis and positively correlated with parts of glycolysis-related genes. DDX54 was also experimental verified that regulate 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, RFX2. The RFX2/LINC00908/DDX54 axis regulated LUAD tumor growth, migration, invasion, cell apoptosis and glycolysis both in vitro and in vivo. These results demonstrated that this axis might be a novel mediator in LUAD progress. We might offer a novel therapeutic target for more precise diagnosis and treatment of LUAD.