The regulatory role and mechanism of LncRNA LUCAT1 mediated miR-199b-5p/MAPKAPK3 axis in the development of papillary thyroid cancer
Objective To explore the effects of lncRNA LUCAT1 on the proliferation,migration,invasion,apoptosis,and EMT of papillary thyroid cancer TPC-1 cells,and further investigate the role of miR-199b-5p/MAPKAPK3 axis in this process.Methods The expressions of LUCAT1,miR-199b-5p,and MAPKAPK3 in papillary thyroid carcinoma and adjacentnormal tissues were detected by RT-qPCR.Bioinformatics predicted the potential binding sites of miR-199b-5p with LUCAT1 or MAPKAPK3,and verified the binding of miR-199b-5p with LUCAT1 or MAPKAPK3 viadouble luciferase reporter gene experiment.TPC-1 cells were divided into sh-NC group,sh-LUCAT1 group,sh-LUCAT1+inhibitor NC group,sh-LUCAT1+miR-199b-5p inhibitor group,and sh-LUCAT1+miR-199b-5p inhibitor+sh-MAPKAPK3 group.The expression of MAPKAPK3 of cells in each group were detected by Western blot.Cell proliferation activity of cells in each group were detected by CCK-8.Apoptosis rate of cells in each group were detected by flow cytometry.The ability of migration and invasion of cells in each group were detected by transwell assay.The expressions of EMT related proteins of cells in each group were detected by Western blot.Results LUCAT1 and MAPKAPK3 were high expression and miR-199b-5p was low expression in papillary thyroid carcinoma tissues.MiR-199b-5p binds to LUCAT1 and MAPKAPK3.Knocking down LUCAT1 reduced the expression of MAPKAPK3,inhibited cell proliferation,migration,invasion,and EMT,and promoted cell apoptosis of TPC-1 cells.Inhibiting miR-199b-5p reversed the inhibitory effect of knockdown LUCAT1 on cell proliferation,migration,invasion,EMT,and the promoting effect of cell apoptosis of TPC-1 cells.Knocking down MAPKAPK3 reversed the inhibitory effect of miR-199b-5p on cell proliferation,migration,invasion,EMT,and apoptosis of TPC-1 cells with knockdown LUCAT1.Conclusion lncRNA LUC AT1 may promote proliferation,migration,invasion,EMT,and inhibit cell apoptosis by competitively binding to miR-199b-5p and upregulating MAPKAPK3 expression.
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