Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α
Abstract 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 ratio...
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| Format: | Article |
| Language: | English |
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Springer
2025-05-01
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| Series: | Discover Oncology |
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| Online Access: | https://doi.org/10.1007/s12672-025-02429-y |
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| author | Liu Jia Fei Yu |
| author_facet | Liu Jia Fei Yu |
| author_sort | Liu Jia |
| collection | DOAJ |
| description | Abstract 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. |
| format | Article |
| id | doaj-art-56a68dc07ec14ff19ac727e6b84be433 |
| institution | Kabale University |
| issn | 2730-6011 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | Springer |
| record_format | Article |
| series | Discover Oncology |
| spelling | doaj-art-56a68dc07ec14ff19ac727e6b84be4332025-08-20T03:53:58ZengSpringerDiscover Oncology2730-60112025-05-0116111010.1007/s12672-025-02429-yOverexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1αLiu Jia0Fei Yu1Department of Pathology, The Second Affiliated Hospital, Zhejiang University School of MedicineDepartment of Pathology, The Second Affiliated Hospital, Zhejiang University School of MedicineAbstract 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.https://doi.org/10.1007/s12672-025-02429-yMAFG-AS1 expressionGlucose metabolism reprogrammingOvarian cancerCell proliferation/growth |
| spellingShingle | Liu Jia Fei Yu Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α Discover Oncology MAFG-AS1 expression Glucose metabolism reprogramming Ovarian cancer Cell proliferation/growth |
| title | Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α |
| title_full | Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α |
| title_fullStr | Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α |
| title_full_unstemmed | Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α |
| title_short | Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α |
| title_sort | overexpression of mafg as1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating hif 1α |
| topic | MAFG-AS1 expression Glucose metabolism reprogramming Ovarian cancer Cell proliferation/growth |
| url | https://doi.org/10.1007/s12672-025-02429-y |
| work_keys_str_mv | AT liujia overexpressionofmafgas1inovariancancerpromotesglucosemetabolismreprogrammingandmalignantbiologicalbehaviorofovariancancercellsbyregulatinghif1a AT feiyu overexpressionofmafgas1inovariancancerpromotesglucosemetabolismreprogrammingandmalignantbiologicalbehaviorofovariancancercellsbyregulatinghif1a |