miR‑592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin‑dependent kinase 8
- Ting Liu
- Jingjing Meng
- Yu Zhang
Affiliations: Department of Nuclear Medicine, The Affiliated Wuhan Central Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China, Department of Thyroid and Breast Surgery, The Affiliated Wuhan Central Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China, Department of Surgery II, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, P.R. China
- Published online on: July 30, 2020 https://doi.org/10.3892/mmr.2020.11392
Copyright: © Liu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Medullary thyroid carcinoma (MTC) is a relatively rare subtype of thyroid cancer, accounting for 5‑10% of all cases of thyroid cancer worldwide. Due to the current lack of knowledge regarding the tumorigenesis of MTC, the clinical treatment of MTC remains a challenge. It has been reported that microRNAs (miRNAs) regulate the progression of MTC; however, the regulatory network of miRNAs and the exact underlying mechanisms are not completely understood. In the present study, an miRNA expression profile (GSE40807), consisting of 80 samples, was downloaded and analyzed using Gene Expression Omnibus‑2R to identify differentially expressed miRNAs between MTC and normal samples. miR‑592 expression levels were significantly increased in MTC tissues and cell lines compared with normal tissues and cell lines. Patients with high miR‑592 expression levels exhibited a less favorable prognosis compared with patients with low miR‑592 expression. The results suggested that miR‑592 overexpression promoted TT and MZ‑CRC‑1 cell proliferation in vitro. In addition, miR‑592 negatively regulated cyclin‑dependent kinase 8 (CDK8) via targeted binding in MTC cells. Moreover, co‑transfection of CDK8 overexpression plasmid and miR‑592 mimic reversed miR‑592‑mediated MTC cell proliferation. In conclusion, miR‑592 may serve as an oncogene in MTC by decreasing the expression of CDK8, indicating that the miR‑592/CDK8 axis might serve as a promising therapeutic target for MTC.