ArticleMolecular biology reports2025
Targeting the lncRNA RBM5-AS1/GCN5 axis under fasting conditions reprograms Glycolysis and induces apoptosis in ovarian cancer cells.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Intermittent fasting synergizes with GCN5 inhibition to suppress RBM5-AS1/GCN5/PGC-1α-driven Warburg metabolism in ovarian cancer.Functional & integrative genomics · 2026Article
- Glycolytic reprogramming in ovarian cancer: mechanisms, immune crosstalk, and therapeutic implications.Frontiers in immunology · 2026Review
- Glycolytic reprogramming in cancer: immune crosstalk, nutrient competition, and supportive care perspectives.Frontiers in immunology · 2026Review
- Proteomic Identification of ALDOA as a Pathogenic TDP-43 Interaction Partner in ALS.Degenerative neurological and neuromuscular disease · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOvarian cancer is a highly aggressive malignancy influenced by complex molecular interactions, including those involving long non-coding RNAs. RBM5-AS1, a nuclear-retained lncRNA, interacts with GCN5 to acetylate PGC-1α, thereby enhancing the Warburg effect. Although fasting is known to exert antitumor effects by modulating lncRNAs and activating PGC-1α, its impact on the RBM5-AS1/GCN5 axis in ovarian cancer remains underexplored. This study evaluates the therapeutic efficacy of RBM5-AS1 knockdown and GCN5 inhibition under fasting-mimicked conditions in SKOV3 cells. METHODS AND
resultsThe findings of cytotoxicity assays revealed a dose-dependent decrease in cell viability, with the fasting + siRNA + MB-3 combination showing the most potent anticancer effect. LDH assays confirmed enhanced membrane damage in this group. Migration assays demonstrated reduced motility, while DAPI and acridine orange/ethidium bromide staining indicated significant apoptotic features present in fasting + siRNA + MB-3-treated ovarian cancer cells. Colony formation was markedly inhibited under the combination treatment, confirming suppression of clonogenic potential. Flow cytometry analysis revealed > 80% late apoptotic/necrotic cells in the fasting + siRNA + MB-3 group. Gene expression analysis further showed downregulation of Warburg-related genes (PDK1/2/3/4, LDH, GLUT1/3/4) and upregulation of PDH and pro-apoptotic markers (Caspase, Bax), alongside reduced PGC-1α acetylation.
conclusionThese findings indicate that fasting enhances the therapeutic effect of RBM5-AS1 knockdown and GCN5 inhibition, leading to a significant disruption of glycolytic metabolism and promoting apoptosis. This combinatorial approach highlights a promising metabolic and epigenetic strategy for ovarian cancer treatment.
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Registered trials
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