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Necroptosis: STAT3 kills?
JAKSTAT. 2012 Jul 1;1(3):200-2. doi: 10.4161/jkst.20968.
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GRIM-19-mediated translocation of STAT3 to mitochondria is necessary for TNF-induced necroptosis.GRIM-19 介导的 STAT3 向线粒体易位是 TNF 诱导的坏死性凋亡所必需的。
J Cell Sci. 2012 Jun 15;125(Pt 12):2995-3003. doi: 10.1242/jcs.103093. Epub 2012 Mar 5.
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Expression of Concern: GRIM-19-mediated translocation of STAT3 to mitochondria is necessary for TNF-induced necroptosis. Nataly Shulga, John G. Pastorino. J Cell Sci doi: 10.1242/jcs.103093.关注声明：GRIM-19介导的STAT3向线粒体的转位对于肿瘤坏死因子诱导的坏死性凋亡是必需的。娜塔莉·舒尔加、约翰·G·帕斯托里诺。《细胞科学杂志》doi: 10.1242/jcs.103093 。
J Cell Sci. 2016 Feb 15;129(4):870. doi: 10.1242/jcs.187013.
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Cytosolic calcium mediates RIP1/RIP3 complex-dependent necroptosis through JNK activation and mitochondrial ROS production in human colon cancer cells.胞质钙通过激活JNK和产生活线粒体ROS介导人结肠癌细胞中RIP1/RIP3复合物依赖性坏死性凋亡。
Free Radic Biol Med. 2017 Jul;108:433-444. doi: 10.1016/j.freeradbiomed.2017.04.010. Epub 2017 Apr 14.
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TRADD Mediates RIPK1-Independent Necroptosis Induced by Tumor Necrosis Factor.TRADD介导肿瘤坏死因子诱导的不依赖RIPK1的坏死性凋亡。
Front Cell Dev Biol. 2020 Jan 22;7:393. doi: 10.3389/fcell.2019.00393. eCollection 2019.
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Curcumol induces RIPK1/RIPK3 complex-dependent necroptosis via JNK1/2-ROS signaling in hepatic stellate cells.姜黄素通过 JNK1/2-ROS 信号通路诱导肝星状细胞中 RIPK1/RIPK3 复合物依赖的坏死性凋亡。
Redox Biol. 2018 Oct;19:375-387. doi: 10.1016/j.redox.2018.09.007. Epub 2018 Sep 7.
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RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome.RIP1 自身磷酸化受线粒体 ROS 促进，并且对于 RIP3 招募到坏死小体中是必需的。
Nat Commun. 2017 Feb 8;8:14329. doi: 10.1038/ncomms14329.
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RIP1-mediated mitochondrial dysfunction and ROS production contributed to tumor necrosis factor alpha-induced L929 cell necroptosis and autophagy.RIP1 介导的线粒体功能障碍和 ROS 产生导致了肿瘤坏死因子-α诱导的 L929 细胞坏死和自噬。
Int Immunopharmacol. 2012 Dec;14(4):674-82. doi: 10.1016/j.intimp.2012.08.003. Epub 2012 Sep 20.
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Shikonin induces glioma cell necroptosis in vitro by ROS overproduction and promoting RIP1/RIP3 necrosome formation.紫草素通过过量产生活性氧和促进RIP1/RIP3坏死小体形成在体外诱导胶质瘤细胞坏死性凋亡。
Acta Pharmacol Sin. 2017 Nov;38(11):1543-1553. doi: 10.1038/aps.2017.112. Epub 2017 Aug 17.
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FasL on the surface of Tag7 (PGRP-S)-activated lymphocytes induces necroptosis in HLA-negative tumor cells with the involvement of lysosomes and mitochondria.Tag7 (PGRP-S) 激活的淋巴细胞表面的 FasL 诱导 HLA 阴性肿瘤细胞发生坏死性凋亡，涉及溶酶体和线粒体。
Biochimie. 2018 Sep;152:174-180. doi: 10.1016/j.biochi.2018.07.003. Epub 2018 Jul 7.
引用本文的文献
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Gentiopicroside-Induced gastric cancer necroptosis via the HIF-1 signaling pathway: A study involving molecular docking and experimental validation.龙胆苦苷通过 HIF-1 信号通路诱导胃癌细胞发生坏死性凋亡：一项涉及分子对接和实验验证的研究。
PLoS One. 2024 Nov 21;19(11):e0311152. doi: 10.1371/journal.pone.0311152. eCollection 2024.
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Receptor interacting protein 1 knockdown induces cell death in liver cancer by suppressing STAT3/ATR activation in a p53-dependent manner.受体相互作用蛋白1基因敲低通过以p53依赖的方式抑制STAT3/ATR激活诱导肝癌细胞死亡。
Am J Cancer Res. 2022 Jun 15;12(6):2594-2611. eCollection 2022.
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Gallic acid induces necroptosis via TNF-α signaling pathway in activated hepatic stellate cells.没食子酸通过肿瘤坏死因子-α信号通路诱导活化的肝星状细胞发生坏死性凋亡。
PLoS One. 2015 Mar 27;10(3):e0120713. doi: 10.1371/journal.pone.0120713. eCollection 2015.
本文引用的文献
1
GRIM-19-mediated translocation of STAT3 to mitochondria is necessary for TNF-induced necroptosis.GRIM-19 介导的 STAT3 向线粒体易位是 TNF 诱导的坏死性凋亡所必需的。
J Cell Sci. 2012 Jun 15;125(Pt 12):2995-3003. doi: 10.1242/jcs.103093. Epub 2012 Mar 5.
2
Inhibition of permeability transition pore opening by mitochondrial STAT3 and its role in myocardial ischemia/reperfusion.线粒体 STAT3 抑制通透性转换孔开放及其在心肌缺血/再灌注中的作用。
Basic Res Cardiol. 2010 Nov;105(6):771-85. doi: 10.1007/s00395-010-0124-1. Epub 2010 Oct 20.
3
Inhibition of STAT3 signaling blocks the anti-apoptotic activity of IL-6 in human liver cancer cells.抑制 STAT3 信号通路可阻断白细胞介素-6 在人肝癌细胞中的抗凋亡活性。
J Biol Chem. 2010 Aug 27;285(35):27429-27439. doi: 10.1074/jbc.M110.142752. Epub 2010 Jun 18.
4
The role of the kinases RIP1 and RIP3 in TNF-induced necrosis.RIP1 和 RIP3 激酶在 TNF 诱导的细胞坏死中的作用。
Sci Signal. 2010 Mar 30;3(115):re4. doi: 10.1126/scisignal.3115re4.
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The molecular regulation of programmed necrotic cell injury.程序性细胞坏死损伤的分子调控。
Trends Biochem Sci. 2010 Aug;35(8):434-41. doi: 10.1016/j.tibs.2010.03.001. Epub 2010 Mar 26.
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Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation.磷酸化驱动的RIP1-RIP3复合物组装调节程序性坏死和病毒诱导的炎症。
Cell. 2009 Jun 12;137(6):1112-23. doi: 10.1016/j.cell.2009.05.037.
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Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha.受体相互作用蛋白激酶-3决定细胞对肿瘤坏死因子-α的坏死反应。
Cell. 2009 Jun 12;137(6):1100-11. doi: 10.1016/j.cell.2009.05.021.
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RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis.RIP3，一种能量代谢调节因子，可将肿瘤坏死因子诱导的细胞死亡从凋亡转变为坏死。
Science. 2009 Jul 17;325(5938):332-6. doi: 10.1126/science.1172308. Epub 2009 Jun 4.
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Tumour necrosis factor and cancer.肿瘤坏死因子与癌症
Nat Rev Cancer. 2009 May;9(5):361-71. doi: 10.1038/nrc2628. Epub 2009 Apr 3.
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Function of mitochondrial Stat3 in cellular respiration.线粒体Stat3在细胞呼吸中的功能。
Science. 2009 Feb 6;323(5915):793-7. doi: 10.1126/science.1164551. Epub 2009 Jan 8.
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