Hsa_circ_0001806 promotes glycolysis and cell progression in hepatocellular carcinoma through miR-125b/HK2

Objective Hepatocellular carcinoma (HCC) is one of the most common malignant tumours and a leading cause of cancer death. Circular RNA (circRNA) has been demonstrated to play an important role in regulating tumour development. The current study aims to explore the specific role of hsa_circ_0001806 during HCC progression. Methods The expression of hsa_circ_0001806 in HCC tissues and cells was measured through qRT-PCR. Cell proliferation, apoptosis and migration were measured using CCK-8 and Annexin V/PI staining kits, and Transwell assay. Bioinformatics prediction and dual-luciferase reporter assay were adopted to explore the mechanism underlying the cell function of hsa_circ_0001806 in HCC cells. In addition, glycolysis was assessed by measuring the glucose uptake, lactate production and ATP level using a glucose assay kit, fluorometric lactate assay kit and ATP detection assay kit. Results Hsa_circ_0001806 was up-regulated in HCC tissues and cells and positively associated with the advanced TNM stage, metastasis and poor overall survival. The overexpression of hsa_circ_0001806 promoted HCC cell proliferation, migration and glycolysis and inhibited cell apoptosis, while the silence of hsa_circ_0001806 showed an opposite effect. Furthermore, hsa_circ_0001806 acted as a sponge of miR-125b to up-regulate hexokinase II (HK2) expression. In addition, the inhibition of miR-125b and HK2 overexpression partly reversed the inhibitory effect of hsa_circ_0001806 silencing on HCC cell proliferation, migration and glycolysis. Conclusion The inhibition of hsa_circ_0001806 suppressed HCC cell proliferation, migration and glycolysis through mediating miR-125b/HK2 axis.

Automated summary

The up-regulation of hsa_circ_0001806 in HCC tissues and cells was associated with advanced disease stage, metastasis, and poor prognosis. Hsa_circ_0001806 promoted HCC cell proliferation, migration, and glycolysis by acting as a sponge of miR-125b to up-regulate HK2 expression. Inhibition of hsa_circ_0001806 suppressed HCC progression through the miR-125b/HK2 axis.