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Cancer Cell. 2017 Feb 13;31(2):208-224. doi: 10.1016/j.ccell.2017.01.003. Epub 2017 Feb 2.
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Metformin: from mechanisms of action to therapies.二甲双胍：从作用机制到治疗方法。
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Ubiquitination in disease pathogenesis and treatment.泛素化在疾病发病机制和治疗中的作用。
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Autodeubiquitination protects the tumor suppressor BAP1 from cytoplasmic sequestration mediated by the atypical ubiquitin ligase UBE2O.自泛素化保护肿瘤抑制因子 BAP1 免于被非典型泛素连接酶 UBE2O 介导的细胞质隔离。
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癌症生物学中的新二重奏：典型的AMPK和非典型的UBE2O。

A new duet in cancer biology: AMPK the typical and UBE2O the atypical.

作者信息

Vila Isabelle K, Song Su Jung, Song Min Sup

机构信息

Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Soonchunhyang Institute of Medi-bio Science, Soonchunhyang University, Cheonan-si, Chungcheongnam-do, Republic of Korea.

出版信息

Mol Cell Oncol. 2017 Mar 17;4(3):e1304846. doi: 10.1080/23723556.2017.1304846. eCollection 2017.

DOI:10.1080/23723556.2017.1304846
PMID:28616582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5462509/
Abstract

() is upregulated in human cancers. We have demonstrated that genetic deletion or pharmacological blockade of reduces tumorigenesis through inhibiting the mammalian target of rapamycin complex 1-hypoxia-inducible factor 1-α pathway. Critically, UBE2O targets adenosine monophosphate (AMP)-activated protein kinase-α 2 (AMPKα2) for ubiquitination and degradation. We thus suggest the UBE2O-AMPKα2 axis as a potential therapeutic target for cancer.

摘要

（）在人类癌症中上调。我们已经证明，基因缺失或药物阻断 通过抑制雷帕霉素复合物1-缺氧诱导因子1-α途径的哺乳动物靶点来减少肿瘤发生。至关重要的是，UBE2O将腺苷单磷酸（AMP）激活的蛋白激酶-α 2（AMPKα2）靶向泛素化和降解。因此，我们认为UBE2O-AMPKα2轴是癌症的潜在治疗靶点。