From Molecular Mechanisms to Treatment Progress of Ovarian Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 842

Special Issue Editor


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Guest Editor
1. Department of Molecular Oncology, British Columbia Cancer Agency, Vancouver, BC, Canada
2. Pathology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt
Interests: sarcoma; ovarian cancers
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Special Issue Information

Dear Colleagues,

Ovarian cancer remains one of the deadliest gynecologic malignancies worldwide, largely due to vague symptoms that often lead to late-stage diagnosis, high recurrence rates, and the development of drug resistance. Understanding the molecular mechanisms that drive ovarian cancer progression has become pivotal for improving diagnosis, prognostication, and treatment strategies. This Special Issue aims to highlight the latest advances in elucidating the molecular underpinnings of ovarian cancer, including genetic and epigenetic alterations, signaling pathway dysregulation, and tumor microenvironment interactions. We also focus on therapeutic opportunities, encompassing targeted therapies, immunotherapies, and combination strategies designed to overcome treatment resistance. Additionally, the identification of novel biomarkers for early detection, disease monitoring, and therapeutic response prediction is emphasized. Contributions may include original research, comprehensive reviews, and perspectives on the development of preclinical models, including patient-derived xenografts and organoids, which are crucial for translational research and drug development. By integrating insights from molecular mechanisms with advances in therapeutic interventions, this Special Issue seeks to provide a comprehensive overview of current progress and future directions in ovarian cancer research. We invite manuscripts that explore innovative approaches to decipher molecular pathways, address challenges in treatment resistance, and propose potential strategies for improving patient outcomes.

Dr. Amal M. El-Naggar
Guest Editor

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Keywords

  • ovarian cancer
  • molecular mechanisms
  • therapeutic targets
  • drug resistance
  • biomarkers
  • preclinical models
  • targeted therapy
  • immunotherapy
  • tumor microenvironment
  • translational research

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Published Papers (2 papers)

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Research

18 pages, 7014 KB  
Article
Combined Effect of Metformin and miR-145/miR-23b Co-Transfection on Proliferation and Progression in 2D and 3D Epithelial Ovarian Cancer Models
by Matías Alfonso Rubio, Eduardo Velásquez, Sofia Antonucci, María José Sánchez and Carmen Romero
Cells 2026, 15(10), 933; https://doi.org/10.3390/cells15100933 (registering DOI) - 19 May 2026
Abstract
Epithelial ovarian cancer (EOC) remains a lethal malignancy requiring novel therapeutic strategies due to high recurrence and chemoresistance. This study evaluated the combined antitumor effect of metformin and the co-transfection of tumor-suppressor microRNAs miR-145 and miR-23b in A2780 and OV90 EOC cell lines [...] Read more.
Epithelial ovarian cancer (EOC) remains a lethal malignancy requiring novel therapeutic strategies due to high recurrence and chemoresistance. This study evaluated the combined antitumor effect of metformin and the co-transfection of tumor-suppressor microRNAs miR-145 and miR-23b in A2780 and OV90 EOC cell lines using both 2D and 3D models. In monolayer cultures, our approach significantly reduced the expression of proliferation markers Ki-67 and c-MYC, and decreased cell migration and invasion in both cell lines compared to controls. In 3D spheroid models, the treatment reduced VEGF secretion and relative spheroid area in A2780 cells, significantly increasing cytotoxicity; however, OV90 spheroids exhibited marked resistance. Fluorescent miRNA tracking revealed that this resistance occurs despite successful intracellular delivery, indicating an intrinsic biological resistance conferred by the 3D microenvironment. Overall, these findings suggest that the combined administration of metformin and miRs effectively limits tumor progression, but also strongly underscore the importance of using complex 3D models to accurately evaluate therapeutic efficacy and intrinsic resistance mechanisms. Full article
(This article belongs to the Special Issue From Molecular Mechanisms to Treatment Progress of Ovarian Cancer)
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31 pages, 16448 KB  
Article
Punicic Acid in Ovarian Cancer: Anticancer Activity and Mechanistic Insights
by Jingjia Mo, Isabella Mendieta, Alexander J. Adams, Katherine Wiest, Hannah Lee, Victoria Gorman, Rachel Koo, Santiago Garcia, Ethan Nguyen, Aaron Lee, Jihua Feng and Zhiqing Huang
Cells 2026, 15(9), 792; https://doi.org/10.3390/cells15090792 - 27 Apr 2026
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Abstract
Ovarian cancer (OC) remains the deadliest gynecological malignancy, with aged tumor microenvironments linked to poorer outcomes. Our prior work identified reduced levels of free fatty acids (FFAs) within tumor-surrounding adipose tissue of aged OC xenograft rats compared to younger counterparts. In this study, [...] Read more.
Ovarian cancer (OC) remains the deadliest gynecological malignancy, with aged tumor microenvironments linked to poorer outcomes. Our prior work identified reduced levels of free fatty acids (FFAs) within tumor-surrounding adipose tissue of aged OC xenograft rats compared to younger counterparts. In this study, we investigated the therapeutic potential of one such FFA, punicic acid (PunA). We evaluated PunA’s effects on OC and normal cell viability and compared its activity with that of its structural isomer, α-eleostearic acid (α-ESA). Both compounds decreased OC cell viability; however, α-ESA was cytotoxic to normal cells, whereas PunA selectively impaired OC cell viability while sparing normal cells. Additionally, PunA enhanced cisplatin efficacy, demonstrating its potential for use in combination therapy to reduce cisplatin dosage and toxicity without compromising antitumor activity. Mechanistically, PunA induced ferroptosis in OC cells while sparing normal cells by differently modulating lipid peroxidation, fatty acid oxidation, and mitochondrial function. Transcriptomic profiling further revealed coordinated gene expression changes associated with oxidative stress and ferroptosis in PunA-treated OC and normal cells. In a preliminary C57BL/6J-ID8 OC mouse model, PunA suppressed tumor growth. Collectively, these findings identify PunA as a promising therapeutic candidate for OC, acting through ferroptosis and mitochondrial dysfunction, and enhancing cisplatin efficacy while sparing normal cells. Full article
(This article belongs to the Special Issue From Molecular Mechanisms to Treatment Progress of Ovarian Cancer)
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