Circular RNA Pvt1 oncogene (CircPVT1) promotes the progression of papillary thyroid carcinoma by activating the Wnt/β-catenin signaling pathway and modulating the ratio of microRNA-195 (miR-195) to vascular endothelial growth factor A (VEGFA) expression

Abstract

Circular RNAs (circRNAs) have been reported to be involved in the progression of papillary thyroid carcinoma (PTC). However, the role of circular RNA Pvt1 oncogene (<i>circPVT1)</i> in PTC has rarely been reported. In this study, we aimed to investigate the function and mechanism of <i>circPVT1</i> in PTC. The expression level of <i>circPVT1, miR-195</i> and <i>VEGFA</i> were determined by reverse transcription‑quantitative PCR (RT‑qPCR). Fisher's exact test was used to analyze the correlation between <i>circPVT1</i> expression and PTC clinical features. Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) staining assay and transwell assay were conducted to evaluate the cell proliferation, migration and invasion ability. Dual-luciferase reporter and Western blot assay were conducted for evaluating the correlation between <i>miR-195</i> and <i>circPVT1</i> or <i>VEGFA</i>. The results of RT-PCR showed that the expression level of <i>circPVT1</i> was significantly upregulated in PTC tissues and cell lines. After downregulating <i>circPVT1</i> expression in PTC cells, the abilities of cell proliferation, migration, and invasion were obviously suppressed, and the Wnt/β-catenin signaling pathway was also repressed. Besides, <i>miR-195</i> could both bind to <i>PVT1</i> and <i>VEGFA</i>, while <i>PVT1</i> could promote the expression of <i>VEGFA</i> by binding to <i>miR-195</i>. Downregulation of <i>VEGFA</i> expression in PTC cells revealed weakened cell proliferation, migration, and invasion capacities, and restrained Wnt/β-catenin signaling pathway. Therefore, we demonstrated that <i>circPVT1</i> could promote <i>VEGFA</i> expression by sponging <i>miR-195. CircPVT1</i> could serve as a molecule sponge for <i>miR-195</i> and mediate the ceRNA network to promote the expression of <i>VEGFA</i>, thus contributed to the malignant progression of PTC.