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活性氧在癌症中的多效功能。

The pleiotropic functions of reactive oxygen species in cancer.

机构信息

Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA.

Perlmutter NYU Cancer Center, New York University Grossman School of Medicine, New York, NY, USA.

出版信息

Nat Cancer. 2024 Mar;5(3):384-399. doi: 10.1038/s43018-024-00738-9. Epub 2024 Mar 22.

DOI:10.1038/s43018-024-00738-9
PMID:38531982
Abstract

Cellular redox homeostasis is an essential, dynamic process that ensures the balance between reducing and oxidizing reactions within cells and thus has implications across all areas of biology. Changes in levels of reactive oxygen species can disrupt redox homeostasis, leading to oxidative or reductive stress that contributes to the pathogenesis of many malignancies, including cancer. From transformation and tumor initiation to metastatic dissemination, increasing reactive oxygen species in cancer cells can paradoxically promote or suppress the tumorigenic process, depending on the extent of redox stress, its spatiotemporal characteristics and the tumor microenvironment. Here we review how redox regulation influences tumorigenesis, highlighting therapeutic opportunities enabled by redox-related alterations in cancer cells.

摘要

细胞氧化还原稳态是一个基本的、动态的过程,它确保了细胞内还原和氧化反应之间的平衡,因此对生物学的各个领域都有影响。活性氧水平的变化会破坏氧化还原稳态,导致氧化或还原应激,从而导致许多恶性肿瘤的发病机制,包括癌症。从转化和肿瘤起始到转移扩散,癌细胞中活性氧的增加可以反转为促进或抑制肿瘤发生过程,这取决于氧化还原应激的程度、其时空特征和肿瘤微环境。在这里,我们综述了氧化还原调控如何影响肿瘤发生,并强调了通过癌细胞氧化还原相关改变带来的治疗机会。

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Science. 2023 Nov 17;382(6672):820-828. doi: 10.1126/science.adf4154. Epub 2023 Nov 2.
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KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance.肺腺癌中 KEAP1 突变促进免疫逃逸和免疫治疗耐药。
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Phase separation of FSP1 promotes ferroptosis.FSP1 的相分离促进了铁死亡。
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The impact of oxidative stress and the NRF2-KEAP1-ARE signaling pathway on anticancer drug resistance.氧化应激和NRF2-KEAP1-ARE信号通路对抗癌药物耐药性的影响。
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Proteomics and cytokine array jointly reveal the role of macrophage proinflammatory shift in liver fibrosis in dairy cows with ketosis.蛋白质组学和细胞因子阵列联合揭示巨噬细胞促炎转变在酮病奶牛肝纤维化中的作用。
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