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

## TL;DR

This study shows that the long noncoding RNA VCAN-AS1 promotes thyroid cancer growth and spread by interacting with miR-374c-3p.

## Contribution

The novel finding is that VCAN-AS1 functions as a competing endogenous RNA by sponging miR-374c-3p to drive thyroid cancer progression.

## Key findings

- VCAN-AS1 overexpression increases thyroid cancer cell proliferation, migration, and invasion.
- VCAN-AS1 competitively binds miR-374c-3p, reversing its tumor-suppressive effects.
- In vivo experiments confirm the oncogenic role of VCAN-AS1 in thyroid cancer.

## Abstract

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.

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.

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.