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.
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.
