Thyroid cancer incidence has been continuity increasing worldwide. Uridine phosphorylase 1 (UPP1) is a protein‐coding gene and has been detected that UPP1 was the higher expression in many solid malignancies, just as head and neck cancers, breast cancer, compared with paired normal tissue. But the act of UPP1 in thyroid cancer is not explicit. In this article, we investigate the function of UPP1 expression in thyroid cancer. The Cancer Genome Atlas (TCGA) unpaired thyroid cancer and normal RNA‐seq data were downloaded, and our paired thyroid cancer and normal samples were analysed by a polymerase chain reaction. The expression of UPP1 was regulated by transfected small interfering RNA, and the function of UPP1 was determined via migration, invasion and cell proliferation assays. Western blot assay was achieved to determine the UPP1 expression correlates with the function of 5‐FU regulate epithelial‐mesenchymal transition. The significant upregulation of UPP1 in thyroid cancer tissues compared with normal thyroid tissues was revealed by our data and TCGA data. UPP1 overexpression was significantly correlated with lymph node metastasis, tumour stage and tumour size. In the cell, experiments showed that UPP1 low expression significantly suppressed the migration, invasion and proliferation. Western blot assay proves the effect of UPP1 expression on 5‐FU regulates epithelial‐mesenchymal transition pathway. UPP1 plays a crucial oncogene in thyroid cancer. Our findings indicate that UPP1 might be a biomarker of thyroid cancer and may act by regulating epithelial‐mesenchymal transition (EMT).

Evidence has been provided that long noncoding RNAs (LncRNAs) play major roles in affecting essential physiological processes, and many of which seem to have functional roles in tumorigenesis and progression. However, the intrinsic molecular mechanism of LncRNAs acting on papillary thyroid carcinoma is not well understood. In the present study, we found that PROX1-AS1 levels were obviously increased in thyroid cancer cells compared with the normal thyroid epithelial cells. Knockdown of PROX1-AS1 gene expression by siRNA could inhibit cell proliferation. Subsequently, we also observed that silencing PROX1-AS1 might inhibit invasion and migration of thyroid cancer cell lines via modulating the expression of epithelial–mesenchymal transition related proteins. In conclusion, our study indicated that LncRNA PROX1-AS1 could promote papillary thyroid carcinoma development and might serve as a potential targeting marker for papillary thyroid carcinoma.