Zeng Xin-Ya, Qiu Xin-Ze, Wu Jiang-Ni, Liang Sheng-Mei, Huang Jie-An, Liu Shi-Quan
Department of Gastroenterology, The Second Affiliated Hospital of Guangxi Medical University, Nanning 530000, Guangxi Zhuang Autonomous Region, China.
Department of Pathology, The Second Affiliated Hospital of Guangxi Medical University, Nanning 530000, Guangxi Zhuang Autonomous Region, China.
World J Gastrointest Oncol. 2023 Jul 15;15(7):1135-1148. doi: 10.4251/wjgo.v15.i7.1135.
Colorectal cancer (CRC) is a common malignancy that has the second highest incidence and mortality rate. Although there are many personalized treatment options for CRC, the therapeutic effects are ultimately limited by drug resistance. Studies have aimed to block the initiation and progression of CRC by inducing cell death to overcome this obstacle. Substantial evidence has indicated that both autophagy and ferroptosis play important regulatory roles in CRC. Autophagy, a lysosome-dependent process by which cellular proteins and organelles are degraded, is the basic mechanism for maintaining cell homeostasis. The duality and complexity of autophagy in cancer therapy is a hot topic of discussion. Ferroptosis, a regulated cell death pathway, is associated with iron accumulation-induced lipid peroxidation. The activation of ferroptosis can suppress CRC proliferation, invasion and drug resistance. Furthermore, recent studies have suggested an interaction between autophagy and ferroptosis. Autophagy can selectively degrade certain cellular contents to provide raw materials for ferroptosis, ultimately achieving antitumor and anti-drug resistance. Therefore, exploring the interaction between autophagy and ferroptosis could reveal novel ideas for the treatment of CRC. In this review, we describe the mechanisms of autophagy and ferroptosis, focusing on their roles in CRC and the crosstalk between them.
结直肠癌（CRC）是一种常见的恶性肿瘤，其发病率和死亡率位居第二。尽管CRC有许多个性化的治疗方案，但治疗效果最终受到耐药性的限制。研究旨在通过诱导细胞死亡来阻断CRC的发生和发展，以克服这一障碍。大量证据表明，自噬和铁死亡在CRC中均发挥重要的调节作用。自噬是一种依赖溶酶体的过程，通过该过程细胞蛋白质和细胞器被降解，是维持细胞稳态的基本机制。自噬在癌症治疗中的双重性和复杂性是一个热门的讨论话题。铁死亡是一种受调控的细胞死亡途径，与铁积累诱导的脂质过氧化有关。铁死亡的激活可抑制CRC的增殖、侵袭和耐药性。此外，最近的研究表明自噬与铁死亡之间存在相互作用。自噬可以选择性地降解某些细胞成分，为铁死亡提供原料，最终实现抗肿瘤和抗耐药性。因此，探索自噬与铁死亡之间的相互作用可能为CRC的治疗揭示新的思路。在这篇综述中，我们描述了自噬和铁死亡的机制，重点关注它们在CRC中的作用以及它们之间的相互作用。
