NR6A1 and neoplasm: Mechanistically, through a series of methods, including bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR, Western blot analysis, and functional rescue experiments, we demonstrated that NR6A1 may promote the expression of HK1 by directly suppressing miR-302a, thereby reprogramming tumor cell glycolysis and enhancing lung adenocarcinoma cell growth.