MiR-200c regulates invasion, proliferation and EMT of anaplastic thyroid cancer cells by targeting parathyroid hormone like hormone

Abstract

This study aimed to explore the specific effect of miR-200c in anaplastic thyroid cancer (ATC). Hth74 and ARO cell lines were used. Proliferation, invasion, and colony formation activities of Hth74 and ARO cell lines affected by miR-200c were studied. Expression of epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Slug, and Snail) in the Hth74 and ARO cell lines were validated by western blot and qRT-PCR. In addition, the regulation of the parathyroid hormone-like hormone (PTHLH) by miR-200c was assessed. Overexpression of miR-200c inhibited the invasion, proliferation, and colony formation of the ATC cell lines, whereas its downregulation achieved the opposite results. PTHLH was found to be regulated negatively by miR-200c through a miR-200c binding site within the 3'-UTR of PTHLH. miR-200c repressed the proliferation, invasion, and EMT process of cells in ATC cell lines by targeting PTHLH post-transcriptionally, which indicates that miR-200c may be a potential target for the treatment of ATC.

Keywords: anaplastic thyroid cancer; miR-200c; microRNAs; polymerase chain reaction; targeted therapies.