癌症中的铁死亡:机制与治疗潜力
Ferroptosis in Cancer: Mechanism and Therapeutic Potential.
作者信息
Singh Mansaa, Arora Hasmiq L, Naik Rutuja, Joshi Shravani, Sonawane Kaveri, Sharma Nilesh Kumar, Sinha Birandra K
机构信息
Cancer and Translational Research Lab, Dr. D.Y. Patil Biotechnology & Bioinformatics Institute, Dr. D.Y. Patil Vidyapeeth, Pune 411033, India.
Mechanistic Toxicology Branch, Division of Translational Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, Durham, NC 27709, USA.
出版信息
Int J Mol Sci. 2025 Apr 18;26(8):3852. doi: 10.3390/ijms26083852.
Cancer drug resistance occurs when cancer cells evade cell death following treatment with chemotherapy, radiation therapy, and targeted therapies. This resistance is often linked to the reprogramming of programmed cell death (PCD) pathways, allowing cancer cells to survive drug-induced stress. However, certain anticancer therapies, when combined with specific agents or inhibitors, can induce ferroptosis-a form of cell death driven by iron-dependent lipid peroxidation. Currently, extensive preclinical and clinical research is underway to investigate the molecular, cellular, and tissue-specific mechanisms underlying ferroptosis, with the goal of identifying strategies to overcome drug resistance in cancers unresponsive to conventional PCD pathways. By harnessing ferroptosis, cancer cells can be compelled to undergo lipid peroxidation-induced death, potentially improving therapeutic outcomes in patients with cancer. This short review aims to enhance the understanding of ferroptosis inducers in cancer therapy and stimulate further research into ferroptosis-based approaches for more effective clinical cancer treatment.
癌症耐药性是指癌细胞在接受化疗、放疗和靶向治疗后逃避细胞死亡的现象。这种耐药性通常与程序性细胞死亡(PCD)途径的重编程有关,使癌细胞能够在药物诱导的应激下存活。然而,某些抗癌疗法与特定的药物或抑制剂联合使用时,可诱导铁死亡——一种由铁依赖性脂质过氧化驱动的细胞死亡形式。目前,正在进行广泛的临床前和临床研究,以探究铁死亡背后的分子、细胞和组织特异性机制,目的是确定克服对传统PCD途径无反应的癌症耐药性的策略。通过利用铁死亡,可以迫使癌细胞经历脂质过氧化诱导的死亡,这可能改善癌症患者的治疗效果。这篇简短的综述旨在加深对癌症治疗中铁死亡诱导剂的理解,并激发对基于铁死亡的方法进行进一步研究,以实现更有效的临床癌症治疗。