文献类型：期刊文献

英文题名：Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives

作者：Han, Yingdi[1];Shen, Xinyu[2];Wang, Kaikai[3];Li, Linzhu[4];Yang, Yufei[5];Suhaimi, Shafinah Ahmad[6];Wei, Yali[3];Zhang, Wenzhi[3];Sun, Kai[7];Li, Zhaoyu[3];Zhang, Haoling[6];Sandai, Doblin[6];He, Yu[8]

第一作者：韩迎娣

通信作者：Li, ZY[1];Zhang, HL[2];Sandai, D[2];He, Y[3]

机构：[1]Gansu Univ Chinese Med, Affiliated Hosp, Dept Obstet & Gynecol, Lanzhou 730020, Gansu, Peoples R China;[2]Naval Med Univ, 800 Xiangyin Rd, Shanghai 200433, Peoples R China;[3]Gansu Univ Chinese Med, Coll Acupuncture Moxibust & Tuina, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[4]Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[5]Gansu Univ Chinese Med, Sch Publ Hlth, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[6]Univ Sains Malaysia, Dept Biomed Sci, Pusat Kanser Tun Abdullah Ahmad Badawi, Kepala Batas 13200, Pulau Pinang, Malaysia;[7]Henan Univ Chinese Med, 156 Jinshui East Rd, Zhengzhou 450000, Henan, Peoples R China;[8]Gansu Univ Chinese Med, Div Acupuncture Rheumatism & Bone Dis, Lanzhou Petrochem Gen Hosp, Affiliated Hosp 4,Dept Tradit Chinese Med, Lanzhou 730060, Gansu, Peoples R China

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Coll Acupuncture Moxibust & Tuina, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Univ Sains Malaysia, Dept Biomed Sci, Pusat Kanser Tun Abdullah Ahmad Badawi, Kepala Batas 13200, Pulau Pinang, Malaysia;[3]corresponding author), Gansu Univ Chinese Med, Div Acupuncture Rheumatism & Bone Dis, Lanzhou Petrochem Gen Hosp, Affiliated Hosp 4,Dept Tradit Chinese Med, Lanzhou 730060, Gansu, Peoples R China.|[10735]甘肃中医药大学;[10735db5df93766a96e5b]甘肃中医药大学针灸推拿学院;

年份：2026

卷号：16

期号：6

起止页码：2407

外文期刊名：AMERICAN JOURNAL OF CANCER RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001814322800018)】；

基金：During manuscript preparation, AI-based tools were used only for language polishing and grammar checking. No AI tools were used to generate scientific content. The authors take full responsibility for the integrity and accuracy of the manuscript. This work was supported by the 2026 Gansu Provincial Traditional Chinese Medicine Gynecology Quality Control Center Project (No. 00213501002) and the Gansu Provincial Capacity Enhancement Project for Advantageous Traditional Chinese Medicine Specialties (Gynecology Specialty Alliance Construction Project) (No. 00213500905) .

语种：英文

外文关键词：Ovarian cancer; ferroptosis; lipid peroxidation; iron homeostasis; therapeutic resistance; precision therapy

摘要：Ovarian cancer is one of the most aggressive malignancies in the female genital system and presents a poor prognosis. Its high rate of recurrence and emergence of acquired resistance to the current chemotherapeutic approaches significantly restrict its long-term therapeutic efficacy. While treatment strategies including cytoreductive surgery (CRS) plus platinum (Pt)-based chemotherapy and poly(ADP-ribose) polymerase inhibitors (PARP inhibitors) have brought clinical benefits to a proportion of patients, the majority eventually suffer cancer relapse post-treatment. This finding suggests that classical forms of cell death may not fully explain treatment outcomes, survival, and resistance in ovarian cancer. Ferroptosis is a nonapoptotic mode of cell death that results from the iron-dependent and lethal peroxidation of lipids. Its onset and progression are contextually regulated by iron homeostasis, lipid metabolism, and redox balance, and also tightly involved in the tumor metabolic reprogramming and adaptation to the tumor microenvironment (TME). Under therapeutic pressure, ovarian cancer cells may become more susceptible to ferroptosis while simultaneously suppressingferroptotic cell death through multilayered regulatory systems, including glutathione peroxidase 4 (GPX4) and the cystine/glutamate antiporter system (system Xc-) antioxidant defenses, acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated lipid peroxidation (LPO), and nuclear receptor coactivator 4 (NCOA4)-dependent ferritinophagy, in order to survive. This biphasic behaviour is strongly linked to treatment resistance and disease recurrence. In this review, the molecular mechanisms by which ferroptosis operates in ovarian cancer are systematically reviewed, and a profile of regulatory factors-genetic, epigenetic, metabolic, and microenvironmental-is presented. Special attention is given to a summary of current literature on the cross-talk between ferroptosis and the sensitivity of Pt-based chemotherapy and PARP inhibitors, cancer stem cell properties within ovarian cancer, as well as the TME. In addition, the current progress in ferroptosis-inducing strategies, nanodelivery systems, and related biomarkers for precision therapy and therapeutic response prediction is comprehensively discussed.