Long noncoding RNA UCA1 promotes anaplastic thyroid cancer cell proliferation via miR‑135a‑mediated c‑myc activation.

Abstract

The long non‑coding RNA (lncRNA), urothelial carcinoma‑associated 1 (UCA1), has been demonstrated to be dysregulated and serves a role in the progression of several cancer types. However, the exact effects and underlying molecular mechanisms of UCA1 in anaplastic thyroid cancer (ATC) remain unknown. The aim of the present study was to investigate the detailed function and the mechanism of UCA1 in the regulation of ATC cell progression. The present study identified that the expression levels of UCA1, in ATC cell lines and tissues, were significantly upregulated compared with normal human thyroid cell line and adjacent non‑cancerous tissues, respectively. UCA1 knockdown significantly inhibited ATC cell viability, proliferation, migration and invasion and the expression level of c‑myc proto‑oncogene (c‑myc) invitro, and suppressed ATC tumor growth invivo. In addition, using luciferase assays, it was confirmed that miR‑135a directly bound to UCA1 and the 3' untranslated region of c‑myc, and UCA1 competed with c‑myc for miR‑135a binding. miR‑135a inhibition may upregulate c‑myc expression, however, the upregulation of c‑myc may be partially reduced by short hairpin UCA1. The present results illustrated that UCA1 promoted ATC cell proliferation through acting as a competing endogenous RNA by binding miR‑135a. In conclusion, in the present study, UCA1 served as an oncogenic long non‑coding RNA promoting ATC cell proliferation and may be a potential target for human ATC treatment.