CircSND1/miR-182-5p Axis Promotes Proliferative and Invasive Abilities of Thyroid Cancer via Binding Targeting MET

Abstract

Objective. To monitor the impacts of circSND1 upon thyroid cancer (TC) tissues and cells and its mechanisms. Methods. Thiazole blue (MTT) was adopted to monitor the impacts of circSND1 upon the proliferative abilities of TPC-1 and SW1736 cells. 5-Bromodeoxyuridine (BrdU) combined with flow cytometry was adopted to monitor the impacts of circSND1 upon the DNA synthesis of TPC-1 and SW1736 cells. We adopted transwell experiment to examine the impacts of circSND1 on cell invasive abilities of TPC-1 and SW1736 cells. The mRNA quantitative levels of circSND1, miR-182-5p, and mesenchymal epidermal transformation factor (MET) in TC tissues were detected by qRT-PCR experiment. We also adopted luciferase assay to verify the targeting interaction between miR-182-5p and MET or miR-182-5p and circSND1. Results. CircSND1 mRNA and MET mRNA were upregulated in thyroid cancer tissues. MiR-182-5p quantification was attenuated in thyroid cancer tissues. Downregulation of circSND1 suppressed TC progression in vivo and in vitro. Furthermore, luciferase report assay uncovered that miR-182-5p was a direct binding target of circSND1 and MET was a direct binding target of miR-182-5p. Besides, circSND1 regulated MET expression and thyroid cancer cell function via binding miR-182-5p. Conclusion. Overexpression of circSND1 in TC tissues and cells facilitates TC tumorigenesis and metastasis via suppressing the quantitative level of miR-182-5p and inducing the upregulation of MET mRNA and protein expression, which expected to offer fresh clues for the administration of TC.