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Updated: Aug 4, 2025

Evaluating the Angiogenetic Properties of Ovarian Cancer Stem-Like Cells using the Three-Dimensional Co-Culture System, NICO-1
Published on: December 5, 2020
Metabolic reprogramming of the ovarian cancer microenvironment in the development of antiangiogenic resistance
Huiran Yue1,2, Xin Lu1,2
1Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, China.
Abstract:
Antiangiogenic therapies, such as treatment with bevacizumab, display modest survival benefits in ovarian cancer (OC) patients. After a transient response, the upregulation of compensatory proangiogenic pathways and the adoption of alternative vascularization processes lead to the development of resistance. Considering the high mortality rate of OC, there is an urgent need to uncover the underlying mechanisms of antiangiogenic resistance for the development of novel and effective treatment strategies. Recent investigations have confirmed that metabolic reprogramming in the tumor microenvironment (TME) exerts an essential effect on tumor aggressiveness and angiogenesis. In this review, we provide an overview of the metabolic crosstalk between OC and the TME, highlighting the regulatory mechanisms underlying the development of antiangiogenic resistance. Metabolic interventions may interrupt this complex and dynamic interactive network, providing a promising therapeutic option to improve clinical outcome in OC patients.
Insights
Antiangiogenic therapies show limited success in ovarian cancer (OC) due to resistance. Targeting metabolic reprogramming in the tumor microenvironment (TME) offers a promising strategy to overcome this resistance and improve patient outcomes.
Area of Science:
- Oncology
- Cancer Biology
- Tumor Microenvironment
Background:
- Antiangiogenic therapies, like bevacizumab, provide modest survival benefits for ovarian cancer (OC) patients.
- Resistance to antiangiogenic therapy develops due to compensatory proangiogenic pathways and alternative vascularization.
- High OC mortality necessitates understanding antiangiogenic resistance mechanisms for new treatments.
Approach:
- This review explores the metabolic crosstalk between OC and the TME.
- It highlights regulatory mechanisms driving antiangiogenic resistance.
- The focus is on how metabolic reprogramming influences tumor aggressiveness and angiogenesis.
Key Points:
- Metabolic reprogramming in the TME is crucial for tumor aggressiveness and angiogenesis.
- Understanding the metabolic interplay is key to overcoming resistance.
- Targeting these metabolic pathways presents a novel therapeutic avenue.
Conclusions:
- Metabolic interventions can disrupt the OC-TME interactive network.
- This disruption may overcome antiangiogenic resistance.
- Metabolic therapies hold promise for improving clinical outcomes in OC patients.
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