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本文引用的文献

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Alternative nuclear functions for NF-κB family members.NF-κB 家族成员的替代核功能。
Am J Cancer Res. 2011;1(4):446-59. Epub 2011 Feb 16.
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NF-κB and cancer: a paradigm of Yin-Yang.核因子-κB与癌症:阴阳范式
Am J Cancer Res. 2011;1(2):192-221. Epub 2010 Dec 6.
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BH3 mimetics activate multiple pro-autophagic pathways.BH3 模拟物激活多种促进自噬的途径。
Oncogene. 2011 Sep 15;30(37):3918-29. doi: 10.1038/onc.2011.104. Epub 2011 Apr 4.
4
Autophagosomal IkappaB alpha degradation plays a role in the long term control of tumor necrosis factor-alpha-induced nuclear factor-kappaB (NF-kappaB) activity.自噬体 IκBα 的降解在肿瘤坏死因子-α诱导的核因子-κB(NF-κB)活性的长期调控中发挥作用。
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Caspase-mediated cleavage of Beclin-1 inactivates Beclin-1-induced autophagy and enhances apoptosis by promoting the release of proapoptotic factors from mitochondria.Caspase 介导的 Beclin-1 切割使 Beclin-1 诱导的自噬失活,并通过促进促凋亡因子从线粒体释放来增强细胞凋亡。
Cell Death Dis. 2010;1(1):e18. doi: 10.1038/cddis.2009.16.
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Exploiting the mitochondrial unfolded protein response for cancer therapy in mice and human cells.利用线粒体未折叠蛋白反应在小鼠和人类细胞中进行癌症治疗。
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7
Heat shock protein 90-mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells.亚硒酸钠诱导 NB4 细胞中热休克蛋白 90 介导的核因子-κB 失活通过 becn1 转录抑制将自噬转换为细胞凋亡。
Mol Biol Cell. 2011 Apr 15;22(8):1167-80. doi: 10.1091/mbc.E10-10-0860. Epub 2011 Feb 23.
8
Principles and current strategies for targeting autophagy for cancer treatment.靶向自噬治疗癌症的原则和当前策略。
Clin Cancer Res. 2011 Feb 15;17(4):654-66. doi: 10.1158/1078-0432.CCR-10-2634.
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The multiple roles of autophagy in cancer.自噬在癌症中的多重作用。
Carcinogenesis. 2011 Jul;32(7):955-63. doi: 10.1093/carcin/bgr031. Epub 2011 Feb 11.
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Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis.激活的 Ras 需要自噬来维持氧化代谢和肿瘤发生。
Genes Dev. 2011 Mar 1;25(5):460-70. doi: 10.1101/gad.2016311. Epub 2011 Feb 11.

自噬和 NF-κB 信号通路在癌细胞中的复杂相互作用。

The complex interplay between autophagy and NF-κB signaling pathways in cancer cells.

出版信息

Am J Cancer Res. 2011;1(5):629-49. Epub 2011 Apr 26.

PMID:21994903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3189824/
Abstract

Tight regulation of both the NF-κB pathway and the autophagy process is necessary for maintenance of cellular homeostasis. Deregulation of both pathways is frequently observed in cancer cells and is associated with tumorigenesis and tumor cell resistance to cancer therapies. Autophagy is involved in several cellular functions regulated by NF-κB including cell survival, differentiation, senescence, inflammation, and immunity. On a molecular level, autophagy and NF-κB share common upstream signals and regulators and can control each other through positive or negative feedback loops, thus ensuring homeostatic responses. Here, we summarize and discuss the most recent discoveries that shed new light on the complex interplay between autophagy and NF-κB signaling pathways; this certainly has functional relevance in tumorigenesis and tumor responses to therapy.

摘要

NF-κB 通路和自噬过程的紧密调节对于维持细胞内稳态是必要的。两条通路的失调在癌细胞中经常观察到,与肿瘤发生和肿瘤细胞对癌症治疗的耐药性有关。自噬参与 NF-κB 调节的几种细胞功能,包括细胞存活、分化、衰老、炎症和免疫。在分子水平上,自噬和 NF-κB 共享共同的上游信号和调节剂,并且可以通过正反馈或负反馈环相互控制,从而确保内稳态反应。在这里,我们总结和讨论了最近的发现,这些发现为自噬和 NF-κB 信号通路之间的复杂相互作用提供了新的认识;这在肿瘤发生和肿瘤对治疗的反应中具有功能相关性。