Circle RNA hsa_circRNA_100290 serves as a ceRNA for miR‐378a to regulate oral squamous cell carcinoma cells growth via Glucose transporter‐1 (GLUT1) and glycolysis

Abstract Aerobic glycolysis (the Warburg effect) is a robust metabolic hallmark of most tumors, including oral squamous cell carcinoma (OSCC). Glucose transporter 1 (GLUT1), a major glucose transporter regulating the glucose uptake, is upregulated in OSCC and participated in the cell glycolysis of OSCC. The deregulation and function of noncoding RNAs in cancers have been widely reported. Reportedly, hsa_circular RNA (circRNA)_100290 (circ_SLC30A7) is significantly upregulated (fold change = 6.91, p < 0.0000001) in OSCC. According to online tools prediction (miRWalk, miRanda, and Targetscan), miR‐378a could simultaneously target circRNA_100290 and GLUT1. Herein, the expression of circRNA_100290 and GLUT1 remarkably increased in oral tumor tissue specimens and cells. In OSCC cell lines, cell proliferation and glycolysis could be remarkably downregulated by circRNA_100290 silence, which could be rescued by GLUT1 overexpression. Conversely, miR‐378a expression could be remarkably inhibited in tumor tissue specimens and cells. The effect of miR‐378a overexpression on OSCC cells was similar to those of circRNA_100290 silence. miR‐378a directly bound to circRNA_100290 and GLUT1 3′‐untranslated region, circRNA_100290 could remarkably relieve miR‐378a‐induced inhibition on GLUT1 via acting as a competing endogenous RNA (ceRNA). miR‐378a inhibition remarkably attenuated the effect of circRNA_100290 silence on cell proliferation and glycolysis in OSCC cell lines. In summary, circRNA_100290 serves as a ceRNA to counteract miR‐378a‐mediated GLUT1 suppression, thus promoting glycolysis and cell proliferation in OSCC. We provide a reliable experimental basis for understanding the mechanism of cell growth and glycolysis deregulation in OSCC.