Lorestani Khadijeh, Ghorbanzade Sara, Rahimi Sania, Fazeli Ramina, Khdakarim Nastaran, Hasanvand Afshin, Hazari Vajihe
Department of Gynecology and Obstructive, Lorestan University of Medical Science, Khorramabad, Iran.
Department of Gynecology and Obstructive, Iran University of Medical Science, Tehran, Iran.
Mol Biotechnol. 2025 Jul 12. doi: 10.1007/s12033-025-01473-x.
Ovarian cancer is a highly heterogeneous malignancy characterized by genetic diversity, clonal evolution, and therapeutic resistance, making it one of the deadliest gynecologic cancers worldwide. Neutrophil extracellular traps (NETs), composed of DNA, histones, and proteases, have emerged as critical mediators of tumor progression. This review comprehensively examines the interplay between neutrophils and ovarian cancer cells, emphasizing the role of NETs in shaping the tumor microenvironment and promoting disease progression. We critically analyze recent literature on the mechanisms by which NETs influence ovarian cancer metastasis, immune evasion, and chemoresistance. Furthermore, we discuss potential therapeutic strategies aimed at targeting NET formation to improve patient outcomes. NETs actively contribute to ovarian cancer progression by fostering a protumorigenic microenvironment, enhancing metastatic potential, and impeding the efficacy of standard therapies. Disrupting NET-associated pathways, including platelet-neutrophil interactions, represents a promising avenue for intervention. Emerging strategies, such as antiplatelet agents, have shown potential in modulating NET activity. However, their clinical application remains in early investigational stages, necessitating further research. This review underscores the pivotal role of NETs in ovarian cancer biology and highlights their potential as therapeutic targets. Although novel approaches, including antiplatelet agents, offer promising avenues for disrupting NET-driven tumor progression, their translational feasibility requires further validation. A deeper understanding of NET-mediated mechanisms could pave the way for innovative therapeutic strategies to enhance ovarian cancer treatment and improve patient survival.
卵巢癌是一种高度异质性的恶性肿瘤，其特征在于基因多样性、克隆进化和治疗抗性，使其成为全球最致命的妇科癌症之一。中性粒细胞胞外陷阱（NETs）由DNA、组蛋白和蛋白酶组成，已成为肿瘤进展的关键介质。本综述全面研究了中性粒细胞与卵巢癌细胞之间的相互作用，强调了NETs在塑造肿瘤微环境和促进疾病进展中的作用。我们批判性地分析了近期关于NETs影响卵巢癌转移、免疫逃逸和化疗耐药性机制的文献。此外，我们讨论了旨在靶向NET形成以改善患者预后的潜在治疗策略。NETs通过促进促肿瘤微环境、增强转移潜能和阻碍标准疗法的疗效，积极促进卵巢癌进展。破坏包括血小板-中性粒细胞相互作用在内的与NET相关的途径，是一种有前景的干预途径。新兴策略，如抗血小板药物，已显示出调节NET活性的潜力。然而，它们的临床应用仍处于早期研究阶段，需要进一步研究。本综述强调了NETs在卵巢癌生物学中的关键作用，并突出了它们作为治疗靶点的潜力。尽管包括抗血小板药物在内的新方法为破坏NET驱动的肿瘤进展提供了有前景的途径，但其转化可行性需要进一步验证。对NET介导机制的更深入理解可为创新治疗策略铺平道路，以加强卵巢癌治疗并提高患者生存率。
