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.
Zhang et al. (Thu,) studied this question.