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本文引用的文献

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Growth differentiation factor-15: a p53- and demethylation-upregulating gene represses cell proliferation, invasion, and tumorigenesis in bladder carcinoma cells.生长分化因子-15:一个由p53和去甲基化上调的基因可抑制膀胱癌细胞的增殖、侵袭及肿瘤发生。
Sci Rep. 2015 Aug 7;5:12870. doi: 10.1038/srep12870.
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NAG-1/GDF15 accumulates in the nucleus and modulates transcriptional regulation of the Smad pathway.NAG-1/GDF15在细胞核中积累并调节Smad信号通路的转录调控。
Oncogene. 2016 Jan 21;35(3):377-88. doi: 10.1038/onc.2015.95. Epub 2015 Apr 20.
3
14-3-3ζ turns TGF-β's function from tumor suppressor to metastasis promoter in breast cancer by contextual changes of Smad partners from p53 to Gli2.14-3-3ζ 通过改变 Smad 伴侣从 p53 到 Gli2,使 TGF-β 的功能从肿瘤抑制因子转变为乳腺癌的转移促进因子。
Cancer Cell. 2015 Feb 9;27(2):177-92. doi: 10.1016/j.ccell.2014.11.025.
4
Wnt/β-Catenin Small-Molecule Inhibitor CWP232228 Preferentially Inhibits the Growth of Breast Cancer Stem-like Cells.Wnt/β-连环蛋白小分子抑制剂 CWP232228 优先抑制乳腺癌干细胞样细胞的生长。
Cancer Res. 2015 Apr 15;75(8):1691-702. doi: 10.1158/0008-5472.CAN-14-2041. Epub 2015 Feb 6.
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Recent advances of p53-MDM2 small molecule inhibitors (2011-present).p53-MDM2小分子抑制剂的最新进展(2011年至今)
Curr Med Chem. 2015;22(5):618-26. doi: 10.2174/0929867322666141128162557.
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Small-molecule inhibitors of the MDM2-p53 protein-protein interaction (MDM2 Inhibitors) in clinical trials for cancer treatment.用于癌症治疗临床试验的MDM2-p53蛋白-蛋白相互作用小分子抑制剂(MDM2抑制剂)。
J Med Chem. 2015 Feb 12;58(3):1038-52. doi: 10.1021/jm501092z. Epub 2014 Nov 14.
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High Mobility Group Box1 (HMGB1) released from cancer cells induces the expression of pro-inflammatory cytokines in peritoneal fibroblasts.癌细胞释放的高迁移率族蛋白B1(HMGB1)可诱导腹膜成纤维细胞中促炎细胞因子的表达。
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癌症中的兼职蛋白

Moonlighting proteins in cancer.

作者信息

Min Kyung-Won, Lee Seong-Ho, Baek Seung Joon

机构信息

Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.

Department of Nutrition and Food Science, College of Agriculture and Natural Resources, University of Maryland, College Park, MD 20742, USA.

出版信息

Cancer Lett. 2016 Jan 1;370(1):108-16. doi: 10.1016/j.canlet.2015.09.022. Epub 2015 Oct 20.

DOI:10.1016/j.canlet.2015.09.022
PMID:26499805
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4684795/
Abstract

Since the 1980s, growing evidence suggested that the cellular localization of proteins determined their activity and biological functions. In a classical view, a protein is characterized by the single cellular compartment where it primarily resides and functions. It is now believed that when proteins appear in different subcellular locations, the cells surpass the expected activity of proteins given the same genomic information to fulfill complex biological behavior. Many proteins are recognized for having the potential to exist in multiple locations in cells. Dysregulation of translocation may cause cancer or contribute to poorer cancer prognosis. Thus, quantitative and comprehensive assessment of dynamic proteins and associated protein movements could be a promising indicator in determining cancer prognosis and efficiency of cancer treatment and therapy. This review will summarize these so-called moonlighting proteins, in terms of a coupled intracellular cancer signaling pathway. Determination of the detailed biological intracellular and extracellular transit and regulatory activity of moonlighting proteins permits a better understanding of cancer and identification of potential means of molecular intervention.

摘要

自20世纪80年代以来,越来越多的证据表明蛋白质的细胞定位决定了它们的活性和生物学功能。传统观点认为,一种蛋白质的特征在于其主要存在和发挥功能的单个细胞区室。现在人们认为,当蛋白质出现在不同的亚细胞位置时,细胞在相同基因组信息的情况下超越了蛋白质的预期活性,以实现复杂的生物学行为。许多蛋白质被认为有可能存在于细胞的多个位置。转运失调可能导致癌症或导致癌症预后较差。因此,对动态蛋白质和相关蛋白质运动进行定量和全面评估可能是确定癌症预后以及癌症治疗和疗法效果的一个有前景的指标。本综述将根据细胞内癌症信号通路的耦合情况总结这些所谓的兼职蛋白。确定兼职蛋白详细的生物细胞内和细胞外转运及调节活性有助于更好地理解癌症并确定潜在的分子干预手段。