LINC00365 inhibited lung adenocarcinoma progression and glycolysis via sponging miR‐429/KCTD12 axis

This study researched the function of long non‐coding RNA LINC00365 in lung adenocarcinoma (LAD) progression. LINC00365, miR‐429, and KCTD12 expression in the LAD clinical tissues and cells were detcetd by qRT‐PCR and Western blot. LINC00365, miR‐429, and KCTD12 effects on H1975 cells malignant phenotype were detected by cell counting kit‐8 assay, clone formation experiment, Transwell experiment, and glycolysis. Dual luciferase reporter gene assay and RNA pull‐down assay were implemented. LINC00365 effect on H1975 cells in vivo growth was detected. LINC00365 was low expressed in the LAD patients and cells, associating with poor outcome. LINC00365 up‐regulation attenuated H1975 cells proliferation, migration, invasion, glycolysis and in vivo growth. LINC00365 inhibited KCTD12 expression by sponging miR‐429. miR‐429 up‐regulation and KCTD12 down‐regulation partial reversed LINC00365 inhibition on H1975 cells malignant phenotype. Thus, LINC00365 inhibited LAD progression and glycolysis via targeting miR‐429/KCTD12 axis. LINC00365 might be a potential candidate for LAD target treatment clinically.