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Research Paper

LncRNA FOXN3-AS2 modulated the growth of papillary thyroid carcinoma via miR-34a/SOX4 axis

Xiao-Song Sun1, Zheng-Chao Wei1, Shuang Liu1, Lei Shi2, Yan-Peng Li1, Ming Wang1
  • 1First Department of Thyroid-Head and Neck Oncosurgery, Jilin Cancer Hospital, Changchun, Jilin Province, China
  • 2Department of Preventive Health Care, Jilin Cancer Hospital, Changchun, Jilin Province, China
Received: February 6, 2021Accepted: May 18, 2021
https://doi.org/10.18632/aging.

Copyright: © 2021 Sun et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.