BioMed Research International · 2020 · 23 citations · 22 references
MedicineMolecular BiologyOncologyGene ExpressionMolecular OncologyNeoplasiaCancer BiomarkersCancer Cell SignalingCancer ProgressionLung CancerMalignant NeoplasmsMolecular Tumor ProfilingCell Viability AssaysColony-forming Unit AssaysDual-luciferase AssaysLuciferase Reporter AssaysLung Squamous Cell CarcinomaMicrorna In CancerMicrorna Regulation In CancerProtein Expression Levels
OBJECTIVE: To investigate the mechanism of miR-30a-5p inhibiting proliferation and migration of lung squamous cell carcinoma (LSCC) cells by targeting FOXD1. METHODS: Bioinformatics was used to analyze differentially expressed genes in the TCGA_LUSC database. qRT-PCR was used to detect the expression levels of miR-30a-5p and FOXD1 in human normal lung epithelial cell line and human LSCC cell lines. The protein expression of FOXD1 was detected by western blot. The cell viability and colony formation abilities were examined by CCK-8 and colony formation assays, respectively. Wound healing and Transwell assays were performed to examine the migration and invasion abilities of cells. The targeted binding sites of miR-30a-5p and FOXD1 were predicted by bioinformatics, and dual luciferase assay was used to verify the targeted binding relationship between miR-30a-5p and FOXD1. RESULT: miR-30a-5p was downregulated in LSCC tissues and cells, while FOXD1 was highly expressed. Overexpression of miR-30a-5p or silencing FOXD1 inhibited cell viability, colony formation ability, migration, and invasion of LSCC cells. miR-30a-5p inhibited the proliferation and migration of LSCC cells by downregulating the expression of FOXD1. CONCLUSION: miR-30a-5p can downregulate the expression of FOXD1 and inhibit the proliferation and migration of LSCC.
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