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本文引用的文献

1
7-Dehydrocholesterol is an endogenous suppressor of ferroptosis.7-脱氢胆固醇是一种内源性的铁死亡抑制剂。
Nature. 2024 Feb;626(7998):401-410. doi: 10.1038/s41586-023-06878-9. Epub 2024 Jan 31.
2
Elevated FSP1 protects KRAS-mutated cells from ferroptosis during tumor initiation.FSP1 升高可保护 KRAS 突变细胞在肿瘤起始时免于发生铁死亡。
Cell Death Differ. 2023 Feb;30(2):442-456. doi: 10.1038/s41418-022-01096-8. Epub 2022 Nov 29.
3
Ferroptosis of tumour neutrophils causes immune suppression in cancer.肿瘤中性粒细胞的铁死亡导致癌症中的免疫抑制。
Nature. 2022 Dec;612(7939):338-346. doi: 10.1038/s41586-022-05443-0. Epub 2022 Nov 16.
4
Curcumin Represses Colorectal Cancer Cell Proliferation by Triggering Ferroptosis PI3K/Akt/mTOR Signaling.姜黄素通过触发铁死亡抑制结直肠癌细胞增殖 PI3K/Akt/mTOR 信号通路。
Nutr Cancer. 2023;75(2):726-733. doi: 10.1080/01635581.2022.2139398. Epub 2022 Nov 8.
5
Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer.靶向从头脂肪生成和 Lands 循环诱导 KRAS 突变型肺癌中的铁死亡。
Nat Commun. 2022 Jul 26;13(1):4327. doi: 10.1038/s41467-022-31963-4.
6
Context-dependent regulation of ferroptosis sensitivity.基于语境的铁死亡敏感性调控。
Cell Chem Biol. 2022 Sep 15;29(9):1409-1418.e6. doi: 10.1016/j.chembiol.2022.06.004. Epub 2022 Jul 8.
7
Development of an Accessible Gene Expression Bioinformatics Pipeline to Study Driver Mutations of Colorectal Cancer.开发一个可访问的基因表达生物信息学管道,以研究结直肠癌的驱动突变。
Altern Lab Anim. 2022 Jul;50(4):282-292. doi: 10.1177/02611929221107546. Epub 2022 Jun 28.
8
Cancer cells dying from ferroptosis impede dendritic cell-mediated anti-tumor immunity.铁死亡导致的癌细胞死亡会抑制树突状细胞介导的抗肿瘤免疫。
Nat Commun. 2022 Jun 27;13(1):3676. doi: 10.1038/s41467-022-31218-2.
9
Mitochondria bridge HIF signaling and ferroptosis blockage in acute kidney injury.线粒体在急性肾损伤中连接 HIF 信号和铁死亡阻断。
Cell Death Dis. 2022 Apr 6;13(4):308. doi: 10.1038/s41419-022-04770-4.
10
Targeting ferroptosis as a vulnerability in cancer.针对癌症中的铁死亡脆弱性。
Nat Rev Cancer. 2022 Jul;22(7):381-396. doi: 10.1038/s41568-022-00459-0. Epub 2022 Mar 25.

结直肠癌中的铁死亡:未来的靶点?

Ferroptosis in colorectal cancer: a future target?

机构信息

Department of Environmental Health Sciences, Yale School of Public Health, Yale University, New Haven, CT, 06510, USA.

Department of Pathology, Yale School of Medicine, New Haven, CT, USA.

出版信息

Br J Cancer. 2023 Apr;128(8):1439-1451. doi: 10.1038/s41416-023-02149-6. Epub 2023 Jan 26.

DOI:10.1038/s41416-023-02149-6
PMID:36703079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10070248/
Abstract

Colorectal cancer (CRC) is the third leading cause of cancer deaths worldwide and is characterised by frequently mutated genes, such as APC, TP53, KRAS and BRAF. The current treatment options of chemotherapy, radiation therapy and surgery are met with challenges such as cancer recurrence, drug resistance, and overt toxicity. CRC therapies exert their efficacy against cancer cells by activating biological pathways that contribute to various forms of regulated cell death (RCD). In 2012, ferroptosis was discovered as an iron-dependent and lipid peroxide-driven form of RCD. Recent studies suggest that therapies which target ferroptosis are promising treatment strategies for CRC. However, a greater understanding of the mechanisms of ferroptosis initiation, propagation, and resistance in CRC is needed. This review provides an overview of recent research in ferroptosis and its potential role as a therapeutic target in CRC. We also propose future research directions that could help to enhance our understanding of ferroptosis in CRC.

摘要

结直肠癌(CRC)是全球癌症死亡的第三大主要原因,其特征是经常发生基因突变,如 APC、TP53、KRAS 和 BRAF。目前的治疗选择包括化疗、放疗和手术,但面临着癌症复发、耐药性和明显毒性等挑战。CRC 治疗通过激活有助于各种形式的受调控细胞死亡(RCD)的生物途径来发挥对癌细胞的疗效。2012 年,铁死亡被发现是一种依赖铁和脂质过氧化物驱动的 RCD 形式。最近的研究表明,针对铁死亡的治疗方法是 CRC 有前途的治疗策略。然而,需要更深入地了解 CRC 中铁死亡的起始、传播和耐药机制。本综述概述了铁死亡的最新研究及其在 CRC 中作为治疗靶点的潜在作用。我们还提出了未来的研究方向,这可能有助于我们加深对 CRC 中铁死亡的理解。