ETS like-1 protein ELK1-induced lncRNA LINC01638 accelerates the progression of papillary thyroid cancer by regulating Axin2 through Wnt/β-catenin signaling pathway

Abstract

ABSTRACT Papillary thyroid carcinoma (PTC) characterized by distant metastasis is a major public health issue among women worldwide. LncRNA LINC01638 is reportedly a critical oncogene in the development of certain cancers. However, the biological function of LINC01638 in PTC is currently unclear. The goal of this study was to identify LINC01638 expression level and its role in PTC progression. The expression of LINC01638 was detected applying qRT-PCR. CCK-8 assay, colony formation assay, immunofluorescence staining and flow cytometric analysis were performed to assess cell proliferation and cell cycle. In addition, cell migration and invasion were examined via wound healing assay, transwell assay and western blot analysis. We found that LINC0163 was upregulated in PTC cells compared with normal thyroid gland epithelial cell line Nthy-ori3-1. ELK1 could act as a transcription factor of LINC01638 and induce LINC01638 expression. LINC01638 silencing inhibited cell proliferation, migration and invasion, and obstructed the progress of TPC-1 cell cycle. LINC0163 silencing activated Axin2 while suppressing the expressions of β-catenin, Cyclin-D1 and c-MYC. Rescue experiment utilizing the transfection of Axin2 overexpression plasmid weakened LINC01638 overexpression-enhanced TPC-1 cell proliferation, metastasis, cell cycle progress and Wnt/β-catenin pathway. These results indicate that LINC0163 regulates PTC progression via inhibition of Wnt/β-catenin and activation of Axin2, which may develop into a novel therapeutic strategy for PTC treatment.