Abstract:
Ferroptosis is a type of cell death that relies on iron and is distinguished by the occurrence of lipid peroxidation and the buildup of reactive oxygen species. Ferroptosis has been demonstrated to have a significant impact on the advancement and resistance to treatment of hepatocellular carcinoma (HCC), thereby highlighting its potential as a viable therapeutic target. Ferroptosis was observed in HCC tissues in contrast to normal liver tissue. The inhibition of ferroptosis has been found to increase the viability of HCC cells and decrease their susceptibility to various anticancer therapies, including chemotherapy, radiotherapy, and immune checkpoint blockade. The administration of drugs that directly modulate ferroptosis regulators or induce excessive production of lipid-reactive oxygen species has demonstrated the potential to enhance the responsiveness of drug-resistant HCC cells to treatment. However, the precise mechanism underlying this phenomenon remains ambiguous. This review presents a comprehensive overview of the crucial role played by ferroptosis in enhancing the efficacy of treatment for hepatocellular carcinoma (HCC). The main aim of this study is to examine the feasibility of utilizing ferroptosis as a therapeutic approach to improve the efficacy of HCC treatment and overcome drug resistance.
摘要:
铁凋亡是一种依赖于铁的细胞死亡,其特征在于脂质过氧化的发生和活性氧的积累。Ferroptosis已被证明对肝细胞癌(HCC)的治疗进展和耐药性有显著影响,从而突出了其作为可行的治疗靶标的潜力。与正常肝组织相比,在HCC组织中观察到铁凋亡。已发现抑制铁凋亡可增加HCC细胞的活力并降低其对各种抗癌疗法的敏感性。包括化疗,放射治疗,和免疫检查点封锁。直接调节铁凋亡调节剂或诱导脂质活性氧物质过量产生的药物的施用已证明了增强耐药HCC细胞对治疗的反应性的潜力。然而,这种现象背后的确切机制仍然模棱两可。这篇综述全面概述了铁凋亡在提高肝细胞癌(HCC)治疗疗效中的关键作用。这项研究的主要目的是研究利用铁性凋亡作为治疗方法的可行性,以提高HCC治疗的疗效并克服耐药性。