Scholarlink

<p>Ferroptosis is an iron-dependent form of regulated cell death characterized by excessive lipid peroxidation. Molecules like GPX4, ACSL4, and SLC7A11 form the core regulatory network. GPX4 inhibits lipid peroxide accumulation, ACSL4 promotes ferroptosis through lipid metabolism remodeling, and SLC7A11 confers resistance to ferroptosis by maintaining redox homeostasis. Ferroptosis has a dual role in cancer: inducing it eliminates cancer cells, while its evasion enhances drug resistance and metastasis. Targeting ferroptosis represents an emerging investigational direction for anticancer therapeutic development, with single-target agents, combination regimens, and nanocarrier-based delivery systems exhibiting preliminary tumor-suppressive signals across diverse preclinical model systems. Despite extensive research, existing reviews lack systematic integration of ferroptosis–tumor microenvironment (TME) crosstalk, comparative analysis of cancer type-specific ferroptosis sensitivity, and critical evaluation of recent clinical progress. This review addresses these gaps by synthesizing molecular mechanisms, cancer-specific roles, TME interactions, and therapeutic applications, along with a critical assessment of clinical translation barriers, providing a framework for ferroptosis-targeted cancer therapy.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Ferroptosis in cancer: molecular mechanisms, biological roles, and therapeutic significance

  • 期刊论文

  • 发表日期：

    2026年4月30日

查看全文
  • Honghua Huang,
  • Jintong Na,
  • Jijie Shao,
  • Qun Yang,
  • Jingyi Su,
  • Yupei Xu,
  • Yongxiang Zhao,
  • Liping Zhong

摘要

Ferroptosis is an iron-dependent form of regulated cell death characterized by excessive lipid peroxidation. Molecules like GPX4, ACSL4, and SLC7A11 form the core regulatory network. GPX4 inhibits lipid peroxide accumulation, ACSL4 promotes ferroptosis through lipid metabolism remodeling, and SLC7A11 confers resistance to ferroptosis by maintaining redox homeostasis. Ferroptosis has a dual role in cancer: inducing it eliminates cancer cells, while its evasion enhances drug resistance and metastasis. Targeting ferroptosis represents an emerging investigational direction for anticancer therapeutic development, with single-target agents, combination regimens, and nanocarrier-based delivery systems exhibiting preliminary tumor-suppressive signals across diverse preclinical model systems. Despite extensive research, existing reviews lack systematic integration of ferroptosis–tumor microenvironment (TME) crosstalk, comparative analysis of cancer type-specific ferroptosis sensitivity, and critical evaluation of recent clinical progress. This review addresses these gaps by synthesizing molecular mechanisms, cancer-specific roles, TME interactions, and therapeutic applications, along with a critical assessment of clinical translation barriers, providing a framework for ferroptosis-targeted cancer therapy.