Background: In recent years, the incidence of thyroid cancer (TC), the most common endocrine malignancy, has been increasing. Emerging evidence indicates that the CUT/CUX/CDP family of proteins can play an important role in tumor development and progression by regulating many cancer-related functions. However, the molecular functions of CUX2  in TC remain unknown. 
Methods: In this study, we used a series of loss-of-function experiments and Western blot analysis to investigate the function of CUX2  in TC and the mechanisms involved. 
Results: Our data revealed that CUX2  expression levels were upregulated in papillary thyroid cancer (PTC). Functionally, CUX2  silencing significantly inhibited PTC cell line (KTC-1 and BCPAP) proliferation, colony formation, migration, invasion, and apoptosis. Furthermore, CUX2  induced epithelial–mesenchymal transition (EMT) and influenced the phosphorylation of AKT and mTOR in the PI3K–AKT–mTOR pathways.
Conclusion: In summary, CUX2  may function as a tumor promoter in TC.
Keywords: papillary thyroid carcinoma, CUX2 , oncogene