Thymosin β10 mediates the effects of microRNA‑184 in the proliferation and epithelial‑mesenchymal transition of BCPAP cells
- Cheng Yang
- Yunni Liu
- Kun Fang
Affiliations: Department of Thyroid and Breast Surgery, The Central Hospital of Wuhan, Wuhan, Hubei 430014, P.R. China, Department of Surgery, Yinchuan Women and Children's Hospital, Yinchuan, Ningxia Hui Autonomous Region 750004, P.R. China
- Published online on: May 11, 2021 https://doi.org/10.3892/etm.2021.10174
Copyright: © Yang
et al. This is an open access article distributed under the
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Thyroid cancer is the most common malignant tumor of the endocrine system. It has been reported that thymosin β10 (TMSB10) serves a vital role in tumor invasion and metastasis, and further understanding the role of TMSB10 in thyroid cancer may provide new insights into the development of novel targeted drugs. Bioinformatics analysis suggested that there might exist a regulatory relationship between miR‑184 and TMSB10. Therefore, the expression of microRNA (miR)‑184 was investigated in the TPC‑1 and BCPAP thyroid cancer cell lines and the Nthy‑ori 3‑1 thyroid epithelial cell line via reverse transcription‑quantitative PCR. The effect of miR‑184 on BCPAP cell proliferation was evaluated using MTT and colony formation assays. In addition, the expression levels of epithelial‑mesenchymal transition (EMT)‑associated proteins were examined via western blot analysis and immunofluorescence staining. Furthermore, the targeting association between miR‑184 and TMSB10 was verified using a dual‑luciferase reporter assay. Notably, miR‑184 overexpression attenuated BCPAP cell proliferation, increased the expression level of the epithelial marker E‑cadherin, and decreased that of the mesenchymal marker vimentin. These effects were reversed in BCPAP cells following TMSB10 overexpression. The present study revealed that TMSB10 may be considered as a key mediator in promoting papillary thyroid carcinoma (PTC) cell proliferation and EMT, which were negatively regulated by miR‑184. Therefore, the findings of the present study may provide a novel potential therapeutic target for attenuating PTC cell proliferation.