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1
YAP/TAZ at the Roots of Cancer.YAP/TAZ与癌症根源
Cancer Cell. 2016 Jun 13;29(6):783-803. doi: 10.1016/j.ccell.2016.05.005.
2
TAZ Protein Accumulation Is Negatively Regulated by YAP Abundance in Mammalian Cells.在哺乳动物细胞中,TAZ蛋白的积累受到YAP丰度的负调控。
J Biol Chem. 2015 Nov 13;290(46):27928-38. doi: 10.1074/jbc.M115.692285. Epub 2015 Oct 2.
3
RUNX3 is a novel negative regulator of oncogenic TEAD-YAP complex in gastric cancer.RUNX3是胃癌中致癌性TEAD-YAP复合物的一种新型负调控因子。
Oncogene. 2016 May 19;35(20):2664-74. doi: 10.1038/onc.2015.338. Epub 2015 Sep 14.
4
RUNX2 and TAZ-dependent signaling pathways regulate soluble E-Cadherin levels and tumorsphere formation in breast cancer cells.RUNX2和TAZ依赖的信号通路调节乳腺癌细胞中可溶性E-钙黏蛋白水平和肿瘤球形成。
Oncotarget. 2015 Sep 29;6(29):28132-50. doi: 10.18632/oncotarget.4654.
5
Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth.YAP/TAZ/TEAD与增强子处的AP-1之间的全基因组关联驱动致癌生长。
Nat Cell Biol. 2015 Sep;17(9):1218-27. doi: 10.1038/ncb3216. Epub 2015 Aug 10.
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The RUNX2 Transcription Factor Negatively Regulates SIRT6 Expression to Alter Glucose Metabolism in Breast Cancer Cells.RUNX2转录因子负向调节SIRT6表达以改变乳腺癌细胞中的葡萄糖代谢。
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Runt-related transcription factor 2 attenuates the transcriptional activity as well as DNA damage-mediated induction of pro-apoptotic TAp73 to regulate chemosensitivity.与 runt 相关的转录因子 2 减弱转录活性以及 DNA 损伤介导的促凋亡 TAp73 的诱导,以调节化学敏感性。
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10
Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells.肿瘤抑制性长链非编码RNA,MT1DP在肝癌细胞中受到YAP和Runx2的负调控,从而抑制叉头框蛋白A1(FoxA1)。
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RUNX在河马通路信号传导中的作用。

Roles of RUNX in Hippo Pathway Signaling.

作者信息

Passaniti Antonino, Brusgard Jessica L, Qiao Yiting, Sudol Marius, Finch-Edmondson Megan

机构信息

Department of Pathology and Marlene & Stewart Greenebaum Comprehensive Cancer Center, University of Maryland School of Medicine, and the Veterans Administration Health Service, Baltimore, MD, USA.

The Mechanobiology Institute (MBI) and the NUS Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Republic of Singapore.

出版信息

Adv Exp Med Biol. 2017;962:435-448. doi: 10.1007/978-981-10-3233-2_26.

DOI:10.1007/978-981-10-3233-2_26
PMID:28299672
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7309331/
Abstract

The Runt-domain (RD) transcription factors (RUNX genes) are an important family of transcriptional mediators that interact with a variety of proteins including the Hippo pathway effector proteins, YAP and TAZ. In this chapter we focus on two examples of RUNX-TAZ/YAP interactions that have particular significance in human cancer. Specifically, recent evidence has found that RUNX2 cooperates with TAZ to promote epithelial to mesenchymal transition mediated by the soluble N-terminal ectodomain of E-Cadherin, sE-Cad. Contrastingly, in gastric cancer, RUNX3 acts as a tumor suppressor via inhibition of the YAP-TEAD complex and disruption of downstream YAP-mediated gene transcription and the oncogenic phenotype. The reports highlighted in this chapter add to the growing repertoire of instances of Hippo pathway crosstalk that have been identified in cancer. Elucidation of these increasingly complex interactions may help to identify novel strategies to target Hippo pathway dysregulation in human cancer.

摘要

Runt结构域(RD)转录因子(RUNX基因)是一类重要的转录调节因子家族,可与多种蛋白质相互作用,包括Hippo信号通路效应蛋白YAP和TAZ。在本章中,我们重点关注RUNX与TAZ/YAP相互作用的两个例子,它们在人类癌症中具有特殊意义。具体而言,最近的证据发现,RUNX2与TAZ协同作用,促进由E-钙黏蛋白可溶性N端胞外域sE-Cad介导的上皮-间质转化。相反,在胃癌中,RUNX3通过抑制YAP-TEAD复合物以及破坏下游YAP介导的基因转录和致癌表型发挥肿瘤抑制作用。本章强调的这些报告增加了在癌症中已确定的Hippo信号通路串扰实例。阐明这些日益复杂的相互作用可能有助于确定针对人类癌症中Hippo信号通路失调的新策略。