Abstract

The incidence of papillary thyroid carcinoma (PTC) has increased gradually, but the reasons are not clear, and the five-year survival rate of late PTC patients is low. Non-coding RNAs were shown to contribute to the progression of multiple cancer, so we aimed to investigate the effect of long noncoding RNA (lncRNA) FOXN3-AS2 on progression, as well as the underlying mechanisms. In the present study, we collected normal and cancer tissues of PTC patients, and found the miR-34a was low expressed in PTC tissues and cells. Upregulation of miR-34a inhibited the progression of PTC cells. SOX4 was the direct target of miR-34a, and FOXN3-AS2 acted as a sponge of miR-153-3p. Forced expression of miR-153-3p or inhibition of SOX4 reversed the effect of FOXN3-AS2 on promoting PTC cells’ migration and invasion. The in vivo tumor growth assay showed that FOXN3-AS2 promoted PTC tumorigenesis by regulating miR-34a/SOX4 axis. In conclusion, FOXN3-AS2 facilitated PTC growth as an oncogene by modulating miR-34a/SOX4 axis, which provides a new molecular mechanism for clinical treatment of PTC.