Conclusion
Therefore, ELF3-AS1 promotes the proliferation of OSCC cells by reprogramming glucose metabolism.
Methods
A total of 112 patients with OSCC were admitted in Guangdong Provincial Stomatological Hospital from March 2016 to March 2019. RT-qPCR, cells and transient transfections, cell proliferation rate measurements and Western blots were carried out to analyze the samples.
Purpose
The present study aims to investigate the role of ELF3-AS1 in oral squamous cell carcinoma (OSCC). Patients and
Results
In the present study, we showed that ELF3-AS1 and glucose transporter 1 (GLUT1) were both upregulated in OSCC tissues, and those two factors were positively correlated. In OSCC cells, ELF3-AS1 overexpression resulted in upregulation, while ELF3-AS1 siRNA silencing caused downregulated expression of GLUT1 and glucose uptake. ELF3-AS1 and GLUT1 overexpression resulted in increased rate of OSCC cells, while ELF3-AS1 and GLUT1 siRNA silencing resulted in decreased proliferation rate of OSCC cells. In addition, GLUT1 siRNA silencing attenuated the effects of ELF3-AS1 overexpression.