Resumen de MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer
C. X. Sun, B. J. Liu, Y. Su, G. W. Shi, Y. Wang, J. F. Chi
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.
