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Updated: Feb 13, 2026

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Prolyl-isomerase Pin1 drives platinum resistance by regulating Notch3 stability and function in ovarian cancer
Maria Valeria Giuli1, Angelica Mancusi2, Bianca Natiello3
1Department of Medico-Surgical Sciences and Biotechnology, Sapienza University of Rome, Laboratory affiliated with Istituto Pasteur Italia- Fondazione Cenci Bolognetti, Latina, Italy.
Background:
Resistance to platinum-based drugs represents a major obstacle for the management of high-grade serous ovarian cancer (HGSOC) patients. Indeed, the selective pressure of platinum-based (PT) chemotherapy often leads to the outgrowth of platinum-resistant subclones. In this scenario, the underlying adaptive networks should be fully investigated to provide advances toward more streamlined and personalized care.
Methods:
We conducted a comprehensive analysis of Pin1/Notch3relationship from HGSOC cell lines and primary tumours, integrating multiple genetic targeting under chemotherapy pressure, differential proteomic approaches, molecular docking data and dynamics simulations, thus identifying a functional circuit evaluated in vitro and in vivo models.We conducted a comprehensive analysis of relationship from HGSOC cell lines and primary tumours, integrating multiple genetic targeting under chemotherapy pressure, differential proteomic approaches, molecular docking data and dynamics simulations, thus identifying a functional circuit evaluated in vitro and in vivo models.
Results:
Here, we demonstrated that carboplatin treatment of HGSOC cells promoted the activation of the Pin1/Notch3 axis, resulting in platinum resistance. Accordingly, HGSOC-bearing patients showing increased Pin1/Notch3 co-expression after PT-based chemotherapy correlated with a clinical worse response. Conversely, genetic targeting of Pin1 combined with carboplatin treatment sensitizes resistant cells to platinum-based therapy, both in vitro and in vivo, strongly reducing their Notch3-mediated metastatic potential in preclinical murine models. Mechanistically, Pin1-Notch3 binding favours protection of Notch3 from its GSK3β-mediated degradation, resulting in increased Notch3 expression.
Conclusions:
Collectively, our findings identify the functional Pin1/Notch3 axis as an escape strategy from chemotherapy-induced cell death, thus suggesting a novel predictive role of the Pin1/Notch3 axis in the platinum response, which could be useful for implementing frontline treatments for HGSOC patients before recurrence.
Insights
The Pin1/Notch3 axis drives platinum resistance in high-grade serous ovarian cancer (HGSOC). Targeting this axis resensitizes tumors to chemotherapy, offering a new strategy for HGSOC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Platinum-based chemotherapy is a cornerstone treatment for high-grade serous ovarian cancer (HGSOC).
- Acquired resistance to platinum drugs is a significant clinical challenge, leading to treatment failure and disease recurrence.
- Understanding the molecular mechanisms underlying platinum resistance is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the role of the Pin1/Notch3 axis in platinum resistance in HGSOC.
- To explore the potential of targeting the Pin1/Notch3 axis to overcome chemotherapy resistance.
- To identify novel predictive biomarkers for platinum response in HGSOC patients.
Main Methods:
- Analysis of Pin1/Notch3 relationship in HGSOC cell lines and primary tumors.
- Genetic targeting of Pin1 and Notch3 in combination with carboplatin treatment.
- Proteomic analysis, molecular docking, and dynamics simulations.
- In vitro and in vivo evaluation in preclinical models.
Main Results:
- Carboplatin treatment activates the Pin1/Notch3 axis, conferring platinum resistance in HGSOC.
- Increased Pin1/Notch3 co-expression in patients correlates with poor response to platinum-based chemotherapy.
- Targeting Pin1 sensitizes resistant HGSOC cells to carboplatin and reduces Notch3-mediated metastasis.
- Pin1 binding protects Notch3 from degradation, leading to increased Notch3 expression.
Conclusions:
- The Pin1/Notch3 axis represents a key escape mechanism from chemotherapy-induced cell death in HGSOC.
- Pin1/Notch3 axis can serve as a predictive biomarker for platinum response.
- Targeting the Pin1/Notch3 axis offers a promising therapeutic strategy for HGSOC patients, potentially before disease recurrence.
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