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本文引用的文献

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Oncogenic hijacking of a developmental transcription factor evokes vulnerability toward oxidative stress in Ewing sarcoma.致癌基因劫持发育转录因子导致尤文肉瘤对氧化应激敏感。
Nat Commun. 2020 May 15;11(1):2423. doi: 10.1038/s41467-020-16244-2.
2
Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes.癌症驱动因素与调控性种系变异的合作塑造了临床结果。
Nat Commun. 2019 Sep 11;10(1):4128. doi: 10.1038/s41467-019-12071-2.
3
Ewing sarcoma.尤因肉瘤。
Nat Rev Dis Primers. 2018 Jul 5;4(1):5. doi: 10.1038/s41572-018-0003-x.
4
Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite.嵌合蛋白EWSR1-FLI1通过GGAA微卫星调控尤文肉瘤易感基因EGR2。
Nat Genet. 2015 Sep;47(9):1073-8. doi: 10.1038/ng.3363. Epub 2015 Jul 27.
5
Clinical and biochemical function of polymorphic NR0B1 GGAA-microsatellites in Ewing sarcoma: a report from the Children's Oncology Group.尤因肉瘤中多态性NR0B1 GGAA微卫星的临床和生化功能:儿童肿瘤学组的报告
PLoS One. 2014 Aug 5;9(8):e104378. doi: 10.1371/journal.pone.0104378. eCollection 2014.
6
Roles of thioredoxin binding protein (TXNIP) in oxidative stress, apoptosis and cancer.硫氧还蛋白结合蛋白 (TXNIP) 在氧化应激、细胞凋亡和癌症中的作用。
Mitochondrion. 2013 May;13(3):163-9. doi: 10.1016/j.mito.2012.06.004. Epub 2012 Jun 27.
7
Elesclomol, counteracted by Akt survival signaling, enhances the apoptotic effect of chemotherapy drugs in breast cancer cells.埃斯克洛莫,通过 Akt 生存信号拮抗作用,增强了乳腺癌细胞中化疗药物的凋亡作用。
Breast Cancer Res Treat. 2010 Jun;121(2):311-21. doi: 10.1007/s10549-009-0470-6. Epub 2009 Jul 16.
8
Elesclomol induces cancer cell apoptosis through oxidative stress.艾力司莫通过氧化应激诱导癌细胞凋亡。
Mol Cancer Ther. 2008 Aug;7(8):2319-27. doi: 10.1158/1535-7163.MCT-08-0298.
9
Sox5 and Sox6 are needed to develop and maintain source, columnar, and hypertrophic chondrocytes in the cartilage growth plate.Sox5和Sox6是软骨生长板中发育和维持源细胞、柱状细胞和肥大软骨细胞所必需的。
J Cell Biol. 2004 Mar 1;164(5):747-58. doi: 10.1083/jcb.200312045.

SOX6:尤因肉瘤的一把双刃剑。

SOX6: a double-edged sword for Ewing sarcoma.

作者信息

Marchetto Aruna, Grünewald Thomas G P

机构信息

Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.

Division of Translational Pediatric Sarcoma Research, German Cancer Research Center (DKFZ), German Cancer Consortium (DKTK), Heidelberg, Germany.

出版信息

Mol Cell Oncol. 2020 Jul 14;7(5):1783081. doi: 10.1080/23723556.2020.1783081. eCollection 2020.

DOI:10.1080/23723556.2020.1783081
PMID:32944640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7469519/
Abstract

Developmental pathways play an important role in cancer. We have recently demonstrated that the constitutive activation of the developmental transcription factor SOX6 via the fusion oncoproteinne EWSR1-FLI1 (Ewing sarcoma breakpoint region 1 - Friend leukemia virus integration 1) contributes to the aggressive phenotype of Ewing sarcoma but on another hand provides an opportunity for targeted therapy.

摘要

发育途径在癌症中起着重要作用。我们最近证明,通过融合癌蛋白EWSR1-FLI1(尤因肉瘤断点区域1-弗瑞德白血病病毒整合1)对发育转录因子SOX6的组成性激活有助于尤因肉瘤的侵袭性表型,但另一方面也为靶向治疗提供了机会。