circCCDC66 promotes thyroid cancer cell proliferation, migratory and invasive abilities and glycolysis through the miR‑211‑5p/PDK4 axis
- Hong Ren
- Zhendi Song
- Chen Chao
- Weizheng Mao
Affiliations: Department of General Surgery, Qingdao Municipal Hospital, Qingdao University School of Medicine, Shandong, Qingdao 266000, P.R. China, Department of General Surgery, Jintan Hospital, Jiangsu University School of Medicine, Changzhou, Jiangsu 213200, P.R. China
- Published online on: March 26, 2021 https://doi.org/10.3892/ol.2021.12677
Copyright: © Ren
et al. This is an open access article distributed under the
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Cancer metastasis is the main cause of death in cancer patients, including patients with thyroid cancer (TC). TC is the most common malignant endocrine tumour. In the recent years, increasing evidence has demonstrated that circular RNAs (circRNAs) serve a significant role in the development of many types of human cancer. However, the function and underlying mechanism of circCCDC66 in TC remain unclear. The present study aimed to explore the role of circCCDC66 in TC. To do so, reverse transcription quantitative PCR was used to detect the expression level of circCCDC66. Cell viability, migratory and invasive abilities, and glucose consumption were evaluated by cell counting kit 8, Transwell and glucose consumption assays, respectively. The association between circCCDC66 or pyruvate dehydrogenase kinase 4 (PDK4) and miR‑211‑5p was verified by dual‑luciferase reporter assay. The results demonstrated that circCCDC66 expression was significantly increased in TC tissues and cell lines. Furthermore, silencing circCCDC66 inhibited TC cell proliferation, migratory and invasive abilities and glycolysis in vitro. Further validation demonstrated that circCCDC66 directly interacted with the microRNA (miR) miR‑211‑5p. Subsequently, the activity of circCCDC66 was attenuated by miR‑211‑5p. In addition, the results demonstrated that circCCDC66 may promote papillary thyroid cancer progression by sponging miR‑211‑5p and increasing expression of PDK4. In conclusion, the present study demonstrated that circCCDC66 could promote TC cell proliferation, migratory and invasive abilities and invasion and glycolysis through the miR‑211‑5p/PDK4 axis. These findings suggested that targeting circCCDC66 may be considered as a promising therapeutic strategy for TC.