The long non‑coding RNA nuclear enrich abundant transcript 1 (NEAT1) has been identified to be carcinogenic in various cancers and elevated NEAT1 expression was tightly linked to tumorigenesis and progression. However, the mechanism has not been revealed in progression of thyroid cancer. Tumor xenograft mouse model was established and tumor size was evaluated. Arg‑1, NEAT1 and miR‑214 expression in CBMs, TAMs, BMDMs and RAW 264.7 cell lines were detected. TPC‑1 cells were subjected to si‑NEAT1 transfection in vitro for cell viability study. A direct target of miRNA‑214 (β‑catenin) was assessed, cell survival and invasion in TAMs were investigated. NEAT1, Arg‑1 was highly expressed and miRNA‑214 had lower expression in patients with thyroid cancer. NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced β‑catenin (a direct target of miRNA‑214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA‑214, presenting a reciprocal repression correlation. In conclusion, these results suggest that high expression of NEAT1 promoted the onset of thyroid carcinoma. In addition, NEAT1 promoted the malignant progression of thyroid cancer through regulating miRNA‑214 expression, which adds to our understanding of the molecular mechanisms in thyroid carcinoma.