LncRNA VCAN‐AS1 Sponges miR‐374c‐3p to Promote Proliferation, Invasion, Migration, and EMT in Thyroid Cancer

Background: Thyroid cancer (TC) is the most common endocrine malignancy worldwide, with a rising incidence in recent years. This study investigates the role of long noncoding RNA VCAN-AS1 (lncRNA VCAN-AS1) in TC cells and its underlying mechanism. Methods and Results: LncRNA sequencing and RT-qPCR revealed that VCAN-AS1 expression in clinical TC tissues was significantly higher than in paracancerous tissues. Methods such as CCK-8, cell scratching, Transwell, and Western Blot were employed to assess the impact of VCAN-AS1 on TC cells. Overexpression of VCAN-AS1 promoted TC cell proliferation, migration, and invasion; downregulated the epithelial-mesenchymal transition (EMT)-related protein E-cadherin; and upregulated N-cadherin, vimentin, slug, and snail. Conversely, silencing VCAN-AS1 reversed these effects. Sequencing identified differentially expressed miR-374c-3p in TC cells between the control and VCAN-AS1 overexpression groups, with functional analysis performed using GO and KEGG pathway enrichment. The regulation of miR-374c-3p by VCAN-AS1 was detected by RT-qPCR in TC cells, and dual-luciferase assays confirmed the binding interaction between VCAN-AS1 and miR-374c-3p. VCAN-AS1 competitively binds with miR-374c-3p, and miR-374c-3p overexpression counteracts VCAN-AS1-induced oncogenic effects. In vivo experiments in mice confirmed the results obtained from in vitro experiments. Conclusion: VCAN-AS1 acts as a competing endogenous RNA, driving TC cell proliferation, migration, invasion, and EMT by sponging miR-374c-3p. These findings contribute to a novel theoretical basis for TC treatment.