Conclusions
This study demonstrated that LINC01410/miR-3619-5p/FOXM1 positive feedback loop regulated cell proliferation and apoptosis in TC, shedding a light on the molecular target identification and promising treatment improvement in TC.
Methods
RT-qPCR and western blot were used to detect gene expression levels. Cell counting kit-8 (CCK-8) and ethynyl-2'-deoxyuridine (EdU) assays were used to determine proliferation. Caspase-3 activity assay was used to examine apoptosis. Intermolecular interaction was investigated by luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay.
Results
We confirmed the elevation of LINC01410 expression in TC cells. Loss-of-function experiments indicated that LINC01410 knockdown suppressed proliferation and facilitated apoptosis in TC. Mechanism research illustrated that LINC01410 positively regulated forkhead box M1 (FOXM1) expression through targeting miR-3619-5p, and that FOXM1 in turn transcriptionally activated LINC01410. Rescue experiments validated that LINC01410 regulated TC proliferation and apoptosis through miR-3619-5p/FOXM1. Conclusions: This study demonstrated that LINC01410/miR-3619-5p/FOXM1 positive feedback loop regulated cell proliferation and apoptosis in TC, shedding a light on the molecular target identification and promising treatment improvement in TC.