Glycolysis-centered understanding of ovarian cancer may support biomarker-guided combination strategies and improve translational therapeutic design
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Key Takeaway
Note that glycolysis-centered understanding may support biomarker-guided strategies but lacks clinical validation.
This narrative review addresses the topic of glycolysis-centered understanding of ovarian cancer. The authors synthesize arguments suggesting that this perspective may support biomarker-guided combination strategies and improve translational therapeutic design. The scope covers potential pathways for future research rather than reporting specific trial data or patient outcomes.
The review highlights several key limitations that affect the certainty of these conclusions. These include metabolic heterogeneity, compensatory pathway activation, limited biomarkers, and insufficient clinical validation. These factors suggest that current evidence is not yet robust enough to drive widespread clinical adoption of specific glycolysis-targeted interventions.
Regarding safety, adverse events, serious adverse events, discontinuations, and tolerability were not reported in this source. The review does not provide specific numerical data on efficacy or safety profiles for any medication.
The practice relevance is that a glycolysis-centered understanding of ovarian cancer may support biomarker-guided combination strategies and improve translational therapeutic design. Clinicians should interpret these findings as conceptual guidance rather than established treatment protocols, given the noted gaps in clinical validation.
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View Original Abstract ↓
Ovarian cancer is characterized by extensive peritoneal dissemination, frequent recurrence, and chemoresistance. Glycolytic reprogramming has emerged as a central metabolic adaptation in ovarian cancer, but its significance extends beyond increased glucose consumption. In this review, we summarize how key glycolytic regulators, including GLUT1, HK2, PFKFB3, PDK1, and LDHA, are controlled by oncogenic, microenvironmental, and non-coding RNA-mediated pathways to reshape tumor metabolism. We emphasize that glycolysis supports ovarian cancer progression by promoting biosynthetic activity, redox balance, invasive dissemination, stem-like plasticity, and therapy resistance. Importantly, this review highlights glycolysis as an immunometabolic regulator of the ovarian tumor microenvironment. Lactate accumulation, macrophage reprogramming, IL-1β/NF-κB signaling, PD-L1 induction, and CD4+ T-cell metabolic remodeling collectively contribute to immune escape. Targeting glycolytic pathways may therefore provide therapeutic opportunities not only to suppress tumor growth but also to enhance chemotherapy and immunotherapy. However, metabolic heterogeneity, compensatory pathway activation, limited biomarkers, and insufficient clinical validation remain major challenges. A glycolysis-centered understanding of ovarian cancer may support biomarker-guided combination strategies and improve translational therapeutic design.
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