LncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway.

Abstract

Thyroid cancer is one of the most common types of cancer in the endocrine system. Among all types of thyroid cancer, papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Long non-coding RNA (lncRNA) BRAF-activated non-protein-coding RNA (BANCR) is a 688-bp-long nucleotide transcript, which was first identified in melanoma. The function of BANCR in thyroid cancer remains unclear. The aim of the present study was to investigate whether BANCR is involved in the development of thyroid cancer. The results indicated that BANCR expression was increased in thyroid tumors compared with in adjacent normal tissues. Among cancer cell lines, the expression level of BANCR differed: BANCR expression in BCPAP cell lines was lower compared with that in CAL-62, WRO and FTC-133 cell lines. Overexpression of BANCR promoted the migration and invasion of BCPAP cells. Additionally, BANCR mediated epithelial-mesenchymal transition (EMT) by regulating the expression of epithelial (E)-cadherin, vimentin and neuronal (N)-cadherin. Overexpression of BANCR in BCPAP cells decreased the expression of E-cadherin and increased the expression of vimentin, N-cadherin, phospho (p)-c-Raf, p-extracellular-signal-regulated kinase (ERK)/mitogen activated protein kinase (MEK)1/2 and p-ERK1/2. Administration of U0126 inhibitor inhibited the regulation of phosphorylation levels by MEK1/2 and ERK1/2. Additionally, U0126 upregulated the expression of E-cadherin and downregulated the expression of vimentin. Taken together, the results of the present study suggest that BANCR induces EMT in PTC through the Raf/MEK/ERK signaling pathway.