In previous studies, numerous dysregulated lncRNAs were identified using RNA-sequencing. Lung cancer is the most common malignant tumour worldwide and the second leading cause in cancer. The aim of this study is to investigate the function and mechanism of lincRNA00858 in the lung cancer. RT-PCR was used to detect the expression of lincRNA00858. Proliferation, invasion, and epithelial-mesenchymal transition (EMT) were examined by CCK8, transwell assay and western blot to evaluate the function of linc00858. Dual-luciferase reporter assay was used to identified the potential target of linc00858. Over-expression of linc00858 significantly promoted cell proliferation, invasion. We also found that linc00858 facilitated the EMT process. Dual-luciferase reporter assay revealed that linc00858 can bind with miR-3182 directly. Linc00858 can negatively regulate the expression of miR-3182. Further experiments demonstrated that MMP2 was the direct target of miR-3182. Rescue experiments revealed that linc00858 functioned through miR-3182/MMP2 axis. Taken together, we verified the role of an unknown linc00858 in lung cancer and provided its mechanism. Mechanistically, linc00858 acted as a competitive endogenous RNA to sponged miR-3182 and regulate MMP2 in lung cancer. Our study provided new clues for understanding the mechanism of lung cancer.
Keywords: EMT; Lung cancer; MMP2; linc00858; miR-3182.