ArticleDiscover oncology2025
Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- A comprehensive review of the emerging role of NRF3 in ovarian cancer tumorigenesis and progression.Journal of ovarian research · 2026Review
- Glycolytic reprogramming in ovarian cancer: mechanisms, immune crosstalk, and therapeutic implications.Frontiers in immunology · 2026Review
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Authors and funding
2 authors.
Funding
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Abstract
objectiveThis research explored the involvement of MAFG-AS1 in metabolic reprogramming and potential molecular mechanisms in ovarian cancer (OC).
methodsThe ability of MAFG-AS1 silencing to affect the glucose intake, lactate production, ECAR, OCR and ATP concentrations and NAD
resultsA 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
conclusionOur 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.
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