Anaplastic thyroid cancer (ATC) remains a cancer with one of the worst prognoses, despite novel targeted therapies. The median survival rate has not improved for decades. Epithelial-to-mesenchymal transition (EMT) is a crucial step in physiological processes and in cancer progression, but the underlying mechanisms are not yet fully understood. The current study examined the role of microRNA (miR)-200b in mesenchymal-to-epithelial transition in ATC. Total RNA and miR isolation were performed from ATC cell lines transfected with a miR-200b mimic. After miR-200b mimic transfection, expression levels of E-cadherin, vimentin and zinc finger E-box binding homeobox 1 (ZEB1) were confirmed by reverse transcription-quantitative PCR and western blotting. Additionally, cell migration was evaluated using miR-200b mimic and scrambled negative control-transfected cells. A total of 14 human ATC and 15 non-cancerous human thyroid tissues were immunohistochemically stained and scored as controls for E-cadherin, vimentin and ZEB1. In ATC tissues and cell lines, the mesenchymal marker ZEB1 was significantly upregulated and the epithelial marker E-cadherin was significantly downregulated. Additionally, the mesenchymal marker vimentin was significantly upregulated in ATC tissues and in one ATC cell line. MiR-200b mimic transfection significantly increased vimentin and ZEB1 expression, but E-cadherin expression remained below the measurement sensitivity. Furthermore, miR-200b overexpression decreased cell migration. The current study suggested that miR-200b may regulate the expression levels of mesenchymal markers such as vimentin and ZEB1 in ATC and may promote mesenchymal-to-epithelial transition.
Keywords: anaplastic thyroid carcinoma; epithelial-to-mesenchymal transition; microRNA 200b; vimentin; zinc finger E-box binding homeobox 1.
Copyright: © Tamagawa et al.