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<p>Ferroptosis, an emerging form of regulated cell death driven by iron-dependent lipid peroxidation, represents a promising therapeutic target in oncology. Gynecological malignancies—cervical, endometrial, and ovarian cancers—are frequently associated with therapeutic resistance due to defective cell death regulation. This review delineates cancer-specific ferroptosis regulatory networks across these malignancies. In cervical cancer, high-risk HPV oncoproteins (E6/E7) rewire oxidative stress and lipid metabolism, leading to stage-dependent ferroptosis vulnerability and supporting combination approaches with immunotherapy. In endometrial cancer, ELK1-mediated GPX4 upregulation drives chemoresistance, highlighting ferroptosis induction as a strategy to overcome treatment failure. In ovarian cancer, iron overload promotes metastasis, while p53, lipid-modifying enzymes (SCD1/FADS2), and the tumor microenvironment (e.g., CXCL8/CXCR2 axis) modulate ferroptosis sensitivity, providing avenues to target aggressive subtypes such as clear cell carcinoma. We conclude that targeting ferroptosis offers a transformative strategy for gynecological cancers.</p>

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Ferroptosis as a novel targeted therapy in gynecological malignant tumors

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月13日

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  • Congxiang Yu,
  • Yuefei Li,
  • Yangxin Fu,
  • Ruizhe Yang,
  • Zorica Nakevska,
  • Pooja Praveen Kumar,
  • An Nhien Tong,
  • Nan Yang,
  • Dan Liu,
  • Chao Chen,
  • Ling Ouyang,
  • Zhijun Xia

摘要

Ferroptosis, an emerging form of regulated cell death driven by iron-dependent lipid peroxidation, represents a promising therapeutic target in oncology. Gynecological malignancies—cervical, endometrial, and ovarian cancers—are frequently associated with therapeutic resistance due to defective cell death regulation. This review delineates cancer-specific ferroptosis regulatory networks across these malignancies. In cervical cancer, high-risk HPV oncoproteins (E6/E7) rewire oxidative stress and lipid metabolism, leading to stage-dependent ferroptosis vulnerability and supporting combination approaches with immunotherapy. In endometrial cancer, ELK1-mediated GPX4 upregulation drives chemoresistance, highlighting ferroptosis induction as a strategy to overcome treatment failure. In ovarian cancer, iron overload promotes metastasis, while p53, lipid-modifying enzymes (SCD1/FADS2), and the tumor microenvironment (e.g., CXCL8/CXCR2 axis) modulate ferroptosis sensitivity, providing avenues to target aggressive subtypes such as clear cell carcinoma. We conclude that targeting ferroptosis offers a transformative strategy for gynecological cancers.