miRNA‑10a promotes cancer cell proliferation in oral squamous cell carcinoma by upregulating GLUT1 and promoting glucose metabolism
- Yuan‑Hua Chen
- Yu Song
- Yan‑Ling Yu
- Wei Cheng
- Xin Tong
Affiliations: Department of Prosthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, P.R. China, Department of Orthodontics, Qingdao Stomatological Hospital, Qingdao, Shandong 266001, P.R. China, Department of Dental Implantation, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, P.R. China
- Published online on: April 16, 2019 https://doi.org/10.3892/ol.2019.10257
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MicroRNA‑10a (miRNA‑10a) promotes lung cancer; however, to the best of our knowledge, its involvement in other cancer types is unknown. The present study aimed to investigate the role of miRNA‑10a in oral cancer. Expression levels of miRNA‑10a and glucose transporter 1 (GLUT1) in tumor tissues and adjacent healthy tissues obtained from patients with oral squamous cell carcinoma (OSCC) were detected by reverse transcription‑quantitative polymerase chain reaction. Correlation analysis between the expression levels of miRNA‑10a and GLUT1 was performed using Pearson's correlation coefficient. It was identified that miRNA‑10a and GLUT1 were upregulated in tumor tissues compared with adjacent healthy tissues of patients with OSCC. Expression levels of miRNA‑10a and GLUT1 were positively correlated in tumor tissues but not in adjacent healthy tissues. In addition, miRNA‑10a overexpression promoted glucose uptake and upregulated GLUT1 in OSCC cells. Furthermore, GLUT1 overexpression promoted glucose uptake; however, no significant increase in the expression level of miRNA‑10a in OSCC cells was detected. Overexpression of miRNA‑10a and GLUT1 promoted OSCC cell proliferation, while GLUT1‑knockdown inhibited OSCC cell proliferation. GLUT1‑knockdown also attenuated the enhancing effect of miRNA‑10a overexpression on cancer cell proliferation. Therefore, miRNA‑10a may promote cancer cell proliferation in OSCC by upregulating GLUT1 and promoting glucose metabolism.