Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α.

OBJECTIVE: This research explored the involvement of MAFG-AS1 in metabolic reprogramming and potential molecular mechanisms in ovarian cancer (OC). METHODS: The ability of MAFG-AS1 silencing to affect the glucose intake, lactate production, ECAR, OCR and ATP concentrations and NAD(+)/NADH ratios in OC cells was examined. Cell cycle phases and apoptosis were measured by flow cytometry. The influences of MAFG-AS1overexprssion on the above assays were also identified. RESULTS: A transient reduction in the number of SKOV3 and HO8910 cells in the MAFG-AS1 knockdown group. MAFG-AS1 knockdown can inhibit cell proliferation, induce apoptosis, and enhance the number of cells in G2 phase. Silencing MAFG-AS1 can inhibit the glucose uptake rate, extracellular lactate production, and ECAR of OC cells, ATP levels, and can promote OCR and NAD(+)/ NADH ratio oxidative phosphorylation. Silencing MAFG-AS1 can inhibit HIF-1α in OC. CONCLUSION: Our study revealed silencing MAFG-AS1 could inhibit the proliferation and induce apoptosis of OC cells by inhibiting the HIF-1α-mediated glycolysis process. Therefore, this study further potentially reveals the machinery of MAFG-AS1 in regulating OC cell proliferation and apoptosis, which is expected to provide a theoretical basis for the study of new targets.