China
Introduction Papillary thyroid cancer (PTC) is the predominant histological type of thyroid cancer, accounting for 80% of thyroid cancers. MiR-181a is a novel microRNA that is usually upregulated in multiple cancers. This study aims to explore the role and underlying mechanism of miR-181a in PTC.
Methods CCK8 and Transwell assays were performed to evaluate cell viability and migration. The mRNA level of miR181a and KLF15 was calculated by qRT-PCR. The protein level of E-Cadherin, N-Cadherin and GAPDH was evaluated by western blot. Dual luciferase assay was conducted to validate that miR-181a directly targeting the 3′-UTR of KLF15 mRNA in TPC-1 cells.
Results We observed that miR-181a was overexpressed and KLF15 was low expressed in PTC tissues and cell lines. Upregulation of miR-181a or downregulation of KLF15 predicted poor outcomes in PTC patients. MiR-181a improved cell growth of PTC, migration and epithelial–mesenchymal transition (EMT) in TPC-1 cells. KLF15 was a target gene of miR-181a and its expression was mediated by miR-181a. KLF15 partially reversed the facilitating efect of miR-181a on cell proliferation and migration in TPC-1 cells.
Conclusion We discovered that miR-181a served as an oncogene downregulating KLF15, thereby inhibiting cell proliferation, migration and the EMT. These fndings demonstrate that miR-181a plays a signifcant role in PTC progression and could be a therapeutic target for PTC.
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