Introduction: Lung cancer (LC) is among the most prevalent malignancies worldwide, with extremely high morbidity and mortality rates. Mounting evidence has suggested that the abnormally expressed long noncoding RNA (lncRNA) in lung cancer tissues may play vital roles in tumor progression. In the present research, we aimed to examine the functions and underlying mechanism of linc01833 in lung adenocarcinoma (LUAD).
Methods: qRT-PCR was employed to determine transfection efficiency. CCK-8, transwell invasion assay, Western blotting analysis and qRT-PCR were used to detect proliferation as well as migration of different LUAD cell lines, and were also applied to determine the changes during epithelial–mesenchymal transformation (EMT). Afterwards, bioinformatics and dual-luciferase reporter assay were utilized to explore and to identify the potential corresponding targets of linc01833 and miR-519e-3p.
Results: Linc01833 OE can significantly improve proliferation as well as invasion ability of LC cells and promote the EMT process. Dual-luciferase reporter assay demonstrated that linc01833 could directly bind to miR-519e-3p, thereby inhibiting its expression. Further experiments showed that S100A4 was a direct target of miR-519e-3p. Rescue assay demonstrated that linc01833 acted on the miR-519e-3p/S100A4 axis.
Conclusion: We verified the mechanism of linc01833 in promoting infiltration and metastasis in LUAD. To be specific, linc01833 can function as a competitive endogenous RNA (ceRNA) to adsorb miR-519e-3p through a sponge and regulate S100A4 in lung cancer, thereby being involved in LUAD progression. Collectively, our research provides new insights towards the in-depth understanding of LC progression mechanisms.
Keywords: lung cancer, linc01833, miR-519e-3p, S100A4, EMT