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蛋白酶体抑制、新癌症疗法的探索和衔接分子 p130Cas。

Proteasome inhibition, the pursuit of new cancer therapeutics, and the adaptor molecule p130Cas.

机构信息

The LeBow Institute for Myeloma Therapeutics and Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.

出版信息

BMC Biol. 2011 Oct 28;9:72. doi: 10.1186/1741-7007-9-72.

DOI:10.1186/1741-7007-9-72
PMID:22034840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3203852/
Abstract

Current interest in proteasome inhibitors for cancer therapy has stimulated considerable research efforts to identify the molecular pathway to their cytotoxicity with a view to identifying the mechanisms of sensitivity and resistance as well as informing the development of new drugs. Zhao and Vuori describe this month in BMC Biology experiments indicating a novel role of the adaptor protein p130Cas in sensitivity to apoptosis induced not only by proteasome inhibitors but also by the unrelated drug doxorubicin.

摘要

目前,蛋白酶体抑制剂在癌症治疗方面受到广泛关注,这激发了大量研究工作,旨在确定其细胞毒性的分子途径,以鉴定敏感性和耐药性的机制,并为新药开发提供信息。Zhao 和 Vuori 在本月的 BMC 生物学杂志上描述了实验结果,该结果表明衔接蛋白 p130Cas 在对蛋白酶体抑制剂和不相关药物阿霉素诱导的细胞凋亡的敏感性中具有新的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b5a/3203852/20645fad829e/1741-7007-9-72-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b5a/3203852/e476db7954ae/1741-7007-9-72-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b5a/3203852/20645fad829e/1741-7007-9-72-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b5a/3203852/e476db7954ae/1741-7007-9-72-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b5a/3203852/20645fad829e/1741-7007-9-72-2.jpg

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Proteasome inhibition, the pursuit of new cancer therapeutics, and the adaptor molecule p130Cas.蛋白酶体抑制、新癌症疗法的探索和衔接分子 p130Cas。
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引用本文的文献

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Sensitization of U937 leukemia cells to doxorubicin by the MG132 proteasome inhibitor induces an increase in apoptosis by suppressing NF-kappa B and mitochondrial membrane potential loss.MG132 蛋白酶体抑制剂对 U937 白血病细胞的增敏作用通过抑制 NF-κB 和线粒体膜电位丧失诱导细胞凋亡增加。
Cancer Cell Int. 2014 Feb 4;14(1):13. doi: 10.1186/1475-2867-14-13.

本文引用的文献

1
The docking protein p130Cas regulates cell sensitivity to proteasome inhibition.对接蛋白 p130Cas 调节细胞对蛋白酶体抑制的敏感性。
BMC Biol. 2011 Oct 28;9:73. doi: 10.1186/1741-7007-9-73.
2
Integrin signalling adaptors: not only figurants in the cancer story.整合素信号衔接蛋白:癌症故事中的不只是配角。
Nat Rev Cancer. 2010 Dec;10(12):858-70. doi: 10.1038/nrc2967. Epub 2010 Nov 24.
3
Proteasome inhibitors activate autophagy as a cytoprotective response in human prostate cancer cells.蛋白酶体抑制剂通过诱导自噬作为一种细胞保护应答激活人前列腺癌细胞。
Oncogene. 2010 Jan 21;29(3):451-62. doi: 10.1038/onc.2009.343. Epub 2009 Nov 2.
4
The double-edged sword of autophagy modulation in cancer.癌症中自噬调节的双刃剑
Clin Cancer Res. 2009 Sep 1;15(17):5308-16. doi: 10.1158/1078-0432.CCR-07-5023. Epub 2009 Aug 25.
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Reversibility of symptomatic peripheral neuropathy with bortezomib in the phase III APEX trial in relapsed multiple myeloma: impact of a dose-modification guideline.在复发多发性骨髓瘤的III期APEX试验中硼替佐米对有症状的周围神经病变的可逆性:剂量调整指南的影响
Br J Haematol. 2009 Mar;144(6):895-903. doi: 10.1111/j.1365-2141.2008.07573.x. Epub 2009 Jan 16.
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Autophagy in the pathogenesis of disease.自噬在疾病发病机制中的作用
Cell. 2008 Jan 11;132(1):27-42. doi: 10.1016/j.cell.2007.12.018.
7
Functions of the proteasome: from protein degradation and immune surveillance to cancer therapy.蛋白酶体的功能:从蛋白质降解、免疫监视到癌症治疗
Biochem Soc Trans. 2007 Feb;35(Pt 1):12-7. doi: 10.1042/BST0350012.
8
Deregulation of proteasome function induces Abl-mediated cell death by uncoupling p130CAS and c-CrkII.蛋白酶体功能失调通过解除p130CAS和c-CrkII的偶联诱导Abl介导的细胞死亡。
J Biol Chem. 2006 Feb 3;281(5):2430-40. doi: 10.1074/jbc.M508454200. Epub 2005 Nov 1.
9
Proteasome inhibition in multiple myeloma: therapeutic implication.蛋白酶体抑制在多发性骨髓瘤中的治疗意义。
Annu Rev Pharmacol Toxicol. 2005;45:465-76. doi: 10.1146/annurev.pharmtox.45.120403.100037.
10
Proteolysis: from the lysosome to ubiquitin and the proteasome.蛋白质水解:从溶酶体到泛素和蛋白酶体。
Nat Rev Mol Cell Biol. 2005 Jan;6(1):79-87. doi: 10.1038/nrm1552.