脂质代谢重编程对卵巢癌生长、转移、耐药的驱动机制与未来挑战
Driving Mechanisms of Lipid Metabolic Reprogramming for Growth, Metastasis, and Drug Resistance in Ovarian Cancer and Future Challenges
投稿时间:2025-07-23  修订日期:2025-11-03
DOI:
中文关键词:  卵巢癌  脂质代谢重编程  TME  化疗耐药  靶向治疗  网膜转移
英文关键词:Ovarian cancer  Lipid metabolism reprogramming  TME  Chemotherapy resistance  Targeted therapy  Omental transfer
基金项目:
作者单位邮编
高吉秘 山西医科大学第二医院 030001
魏芳* 山西医科大学第二医院 030001
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中文摘要:
      卵巢癌作为病死率居妇科恶性肿瘤首位的疾病,其治疗困境主要源于晚期诊断、化疗耐药及高复发率。近年研究发现,脂质代谢重编程通过提供合成原料、能量供应及激活增殖信号通路,驱动卵巢癌恶性进展,同时参与肿瘤微环境(Tumor micro-environment, TME)互作,尤其是与大网膜脂肪细胞的代谢串扰,介导化疗耐药。本文系统综述脂质代谢异常在卵巢癌细胞增殖、凋亡、迁移侵袭及耐药中的双重作用机制,提出靶向脂质合成关键酶(如FASN、ACSL4、CPT1A)及联合铁死亡诱导剂的治疗新策略,并强调基于代谢标志物(胆固醇、PUFA等)的早期诊断价值。未来需深入解析脂质代谢网络交互机制,推动多靶点联合疗法及中医药协同干预的临床转化。
英文摘要:
      Ovarian cancer, the gynecological malignancy with the highest mortality rate, faces treatment challenges primarily due to late-stage diagnosis, chemoresistance, and high recurrence rates. In recent years, it has been found that lipid metabolism reprogramming drives the malignant progress of ovarian cancer by providing biosynthetic precursors, energy supply, and activating proliferation signal pathways, while also participating in interactions with Tumor micro-environment (TME), particularly through metabolic crosstalk with omental adipocytes, and contributing to chemoresistance. This review systematically summarizes the dual roles of lipid metabolic abnormalities in ovarian cancer cell proliferation, apoptosis, migration, invasion, and drug resistance, and proposes novel therapeutic strategies targeting key lipid synthesis enzymes (such as FASN, ACSL4, and CPT1A) in combination with ferroptosis inducers. Additionally, it highlights the potential of metabolism-based biomarkers (e.g., cholesterol, PUFA) for early diagnosis. Future research should further elucidate the interactive networks of lipid metabolism to promote the clinical translation of multi-target combined therapies and integrative interventions involving traditional Chinese medicine.
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