Purpose: The aim of this study was to study the roles and potential mechanism of LINC00520 in the progression of lung cancer.
Methods: The expression of LINC00520 and miR-3175 in lung cancer tissues and cells was detected by qRT-PCR. The disease stage and aggressive of patients were also recorded, and their relationship with LINC00520 level was also calculated. Kaplan–Meier survival curve was drawn to observe the survival difference between high and low expression patients. Lipofectamine 2000 was used to transfect siLINC00520, miR-3175 inhibitor and their controls in lung cancer cells. CCK8 and colony formation assay were processed for cell proliferation. Transwell assay was undertaken for migration and invasion of lung cancer cells. MiRDB predicts the combination of LINC00520 and miR-3175. Luciferase and RNA pulldown assay were applied to verify the binding site. Correlation analysis of miR-3175 and LINC00520 expression in lung cancer tissues was shown.
Results: LINC00520 was highly expressed in lung cancer tissues and cells. Patients at III+IV stage were always with higher LINC00520 level than patients at I+II stage. Patients with high expression of lncRNA LINC00520 have short survival time (hazard ratio=1.7). Knockdown of LINC00520 inhibited proliferation, invasion and migration of lung cancer cells. LINC00520 targeted and negatively regulated miR-3175 (r=− 0.528; P< 0.001). MiR-3175 inhibitor rescued the effect of si-LINC00520 on lung cancer progression.
Conclusion: LncRNA LINC00520 could predict poor prognosis and promote progression of lung cancer by inhibiting miR-3175 expression.
Keywords: lncRNA LINC00520, lung cancer, prognosis, miR-3175