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本文引用的文献

1
E2F transcription factors and digestive system malignancies: how much do we know?E2F 转录因子与消化系统恶性肿瘤:我们了解多少?
World J Gastroenterol. 2013 Jun 7;19(21):3189-98. doi: 10.3748/wjg.v19.i21.3189.
2
The E2F transcription factor 1 transactives stathmin 1 in hepatocellular carcinoma.E2F 转录因子 1 反式激活 stathmin 1 在肝癌中的作用。
Ann Surg Oncol. 2013 Nov;20(12):4041-54. doi: 10.1245/s10434-012-2519-8. Epub 2012 Aug 22.
3
E2F-1 is overexpressed and pro-apoptotic in human hepatocellular carcinoma.E2F-1 在人肝癌中过表达并具有促凋亡作用。
Virchows Arch. 2012 May;460(5):439-46. doi: 10.1007/s00428-012-1220-4. Epub 2012 Mar 27.
4
The dark side of E2F1: in transit beyond apoptosis.E2F1 的阴暗面:在凋亡之外的运输过程中。
Cancer Res. 2012 Feb 1;72(3):571-5. doi: 10.1158/0008-5472.CAN-11-2575.
5
A potential oncogenic role of the commonly observed E2F5 overexpression in hepatocellular carcinoma.E2F5 过表达在肝细胞癌中具有潜在致癌作用。
World J Gastroenterol. 2011 Jan 28;17(4):470-7. doi: 10.3748/wjg.v17.i4.470.
6
Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer.突变型 p53 驱动胰腺癌转移并克服生长停滞/衰老。
Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):246-51. doi: 10.1073/pnas.0908428107. Epub 2009 Dec 14.
7
Emerging roles of E2Fs in cancer: an exit from cell cycle control.E2F蛋白在癌症中的新作用:从细胞周期调控中脱离
Nat Rev Cancer. 2009 Nov;9(11):785-97. doi: 10.1038/nrc2696.
8
Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas.DNA损伤反应机制对E2F1驱动的癌细胞命运的调控以及骨肉瘤中潜在的新型E2F1靶点
Am J Pathol. 2009 Jul;175(1):376-91. doi: 10.2353/ajpath.2009.081160. Epub 2009 Jun 18.
9
E2F1 inhibits c-Myc-driven apoptosis via PIK3CA/Akt/mTOR and COX-2 in a mouse model of human liver cancer.在人肝癌小鼠模型中,E2F1通过PIK3CA/Akt/mTOR和COX-2抑制c-Myc驱动的细胞凋亡。
Gastroenterology. 2008 Oct;135(4):1322-32. doi: 10.1053/j.gastro.2008.07.012. Epub 2008 Jul 17.
10
PEG10 directly regulated by E2Fs might have a role in the development of hepatocellular carcinoma.由E2Fs直接调控的PEG10可能在肝细胞癌的发展中起作用。
FEBS Lett. 2008 Aug 6;582(18):2793-8. doi: 10.1016/j.febslet.2008.07.009. Epub 2008 Jul 14.

E2F转录因子与消化系统恶性肿瘤:我们了解多少?

E2F transcription factors and digestive system malignancies: how much do we know?

作者信息

Evangelou Konstantinos, Havaki Sophia, Kotsinas Athanassios

机构信息

Konstantinos Evangelou, Sophia Havaki, Athanassios Kotsinas, Laboratory Histology-Embryology, Medical School, National and Kapodistrian University of Athens, 11527 Goudi, Athens, Greece.

出版信息

World J Gastroenterol. 2014 Aug 7;20(29):10212-6. doi: 10.3748/wjg.v20.i29.10212.

DOI:10.3748/wjg.v20.i29.10212
PMID:25110451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4123353/
Abstract

The E2F proteins comprise a family of 8 members that function as transcription factors. They are key targets of the retinoblastoma protein (RB) and were initially divided into groups of activators and repressors. Accumulating data suggest that there is no specific role for each individual E2F member. Instead, each E2F can exert a variety of cellular effects, some of which represent opposing ones. For instance, specific E2Fs can activate transcription and repression, promote or hamper cell proliferation, augment or inhibit apoptosis, all being dependent on the cellular context. This complexity reflects the importance that these transcription factors have on a cell's fate. Thus, delineating the specific role for each E2F member in specific malignancies, although not easy, is a challenging and continuously pursued task, especially in view of potential E2F targeted therapies. Therefore, several reviews are continuously trying to evaluate available data on E2F status in various malignancies. Such reviews have attempted to reach a consensus, often in the simplistic form of oncogenes or tumor suppressor genes for the E2Fs. However they frequently miss spatial and temporal alterations of these factors during tumor development, which should also be considered in conjunction with the status of the regulatory networks that these factors participate in. In the current ''Letter to the Editor'', we comment on the flaws, misinterpretations and omissions in one such review article published recently in the World Journal of Gastroenterology regarding the role of E2Fs in digestive system malignancies.

摘要

E2F蛋白家族由8个成员组成,它们作为转录因子发挥作用。它们是视网膜母细胞瘤蛋白(RB)的关键靶点,最初被分为激活因子和抑制因子两组。越来越多的数据表明,每个E2F成员并没有特定的作用。相反,每个E2F都可以发挥多种细胞效应,其中一些效应是相反的。例如,特定的E2F可以激活转录和抑制转录,促进或阻碍细胞增殖,增强或抑制细胞凋亡,所有这些都取决于细胞环境。这种复杂性反映了这些转录因子对细胞命运的重要性。因此,尽管不容易,但确定每个E2F成员在特定恶性肿瘤中的具体作用是一项具有挑战性且一直在进行的任务,特别是考虑到潜在的E2F靶向治疗。因此,有几篇综述不断试图评估各种恶性肿瘤中E2F状态的现有数据。这类综述试图达成共识,通常以E2F作为癌基因或肿瘤抑制基因这种简单的形式。然而,它们经常忽略这些因子在肿瘤发生过程中的时空变化,而这些变化也应结合这些因子所参与的调控网络的状态来考虑。在当前的“致编辑的信”中,我们对最近发表在《世界胃肠病学杂志》上的一篇关于E2F在消化系统恶性肿瘤中作用的综述文章中的缺陷、误解和遗漏进行评论。