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OTULIN将WNT信号传导与三阴性乳腺癌的耐药性联系起来。

OTULIN couples WNT signaling to resistance in triple-negative breast cancer.

作者信息

Wang Wei, Wu Zhao-Hui

机构信息

Department of Radiation Oncology, University of Tennessee Health Science Center, Memphis, TN, USA.

Department of Pathology and Laboratory Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.

出版信息

Mol Cell Oncol. 2020 Oct 15;7(6):1825904. doi: 10.1080/23723556.2020.1825904. eCollection 2020.

Abstract

Oncogenic Wnt/β-catenin activation promotes cancer development and drug resistance to cancer treatments. We recently revealed an underlying mechanism linking linear ubiquitination with Wnt/β-catenin activation upon genotoxic treatments. We showed that ABL1 (ABL proto-oncogene 1)-dependent phosphorylation of OTULIN (OTU deubiquitinase with linear linkage specificity) upon DNA damage drives β-catenin activation which promotes drug resistance in triple-negative breast cancer.

摘要

致癌性Wnt/β-连环蛋白激活促进癌症发展和对癌症治疗的耐药性。我们最近揭示了一种在基因毒性治疗后将线性泛素化与Wnt/β-连环蛋白激活联系起来的潜在机制。我们发现,DNA损伤后,ABL1(ABL原癌基因1)依赖的OTULIN(具有线性连接特异性的OTU去泛素酶)磷酸化驱动β-连环蛋白激活,从而促进三阴性乳腺癌的耐药性。

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The plot thickens: OTULIN regulation in cell death.情况愈发复杂:OTULIN在细胞死亡中的调控。
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本文引用的文献

1
3
Senescence-associated reprogramming promotes cancer stemness.衰老相关重编程促进癌症干性。
Nature. 2018 Jan 4;553(7686):96-100. doi: 10.1038/nature25167. Epub 2017 Dec 20.
6
Molecular basis and regulation of OTULIN-LUBAC interaction.OTULIN-LUBAC 相互作用的分子基础与调控。
Mol Cell. 2014 May 8;54(3):335-48. doi: 10.1016/j.molcel.2014.03.018. Epub 2014 Apr 10.

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