LINC00312 Inhibits Lung Cancer Progression through the miR-3175/SEMA6A Axis.

Abstract

This study aims to clarify molecular mechanisms and tumor-associated functions of LINC00312 in lung cancer. GEO database was used to acquire lung cancer-related expression microarrays. Then, relevant databases were applied to predict the downstream miRNA for LINC00312 and the target mRNA for the potential miRNA, with their associations deeply confirmed through dual-luciferase and RIP assays. The expression levels of epithelial-mesenchymal transition -related proteins (N-cadherin, Vimentin, MMP-2, and MMP-9) were examined by Western blot. The proliferation, migration, and invasion were evaluated through in vitro experiments including CCK-8 and Transwell assays and further validated by nude mouse xenograft tumor experiment. LINC00312, serving as a tumor suppressor, was down-regulated in lung cancer cells. RIP assay proved that miR-3175 bound LINC00312 and SEMA6A. The dual-luciferase assay showed that miR-3175 specifically targeted SEMA6A, suppressing the expression of SEMA6A. Overexpressing LINC00312 remarkably inhibited the binding between miR-3175 and SEMA6A. Overexpressing miR-3175 or silencing SEMA6A could hamper the effects of LINC00312 on lung cancer cells. LINC00312 inhibits lung cancer occurrence and progression via the miR-3175/SEMA6A axis.