MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer

• C. X. Sun ^[2] ; B. J. Liu ^[3] ; Y. Su ^[4] ; G. W. Shi ^[5] ; Y. Wang ^[5] ; J. F. Chi ^[1]
  1. [1] Jinan Central Hospital

     Jinan Central Hospital

     China

     
  2. [2] Department of Endocrinology, Yantaishan Hospital, Yantai 264000, Shandong, China
  3. [3] Operation Room, Rizhao Hospital of TCM, Rizhao 276800, Shandong, China
  4. [4] Operation Room, Qingdao Hospital of Traditional Chinese Medicine, Qingdao Hiser Hospital, Qingdao 266033, Shandong, China
  5. [5] Health Management Center, Zhangqiu District People’s Hospital, Jinan 250200, Shandong, China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 24, Nº. 1 (Enero), 2022, págs. 66-75
• Idioma: inglés
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• Resumen

  • 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.