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本文引用的文献

1
PI3K independent activation of mTORC1 as a target in lapatinib-resistant ERBB2+ breast cancer cells.PI3K 非依赖性激活 mTORC1 作为拉帕替尼耐药的 ERBB2+乳腺癌细胞的靶点。
Breast Cancer Res Treat. 2012 Dec;136(3):683-92. doi: 10.1007/s10549-012-2252-9. Epub 2012 Oct 23.
2
Lapatinib and obatoclax kill breast cancer cells through reactive oxygen species-dependent endoplasmic reticulum stress.拉帕替尼和 obatoclax 通过活性氧依赖的内质网应激杀死乳腺癌细胞。
Mol Pharmacol. 2012 Dec;82(6):1217-29. doi: 10.1124/mol.112.081539. Epub 2012 Sep 18.
3
Temporal profiling of lapatinib-suppressed phosphorylation signals in EGFR/HER2 pathways.EGFR/HER2 通路中拉帕替尼抑制的磷酸化信号的时程分析。
Mol Cell Proteomics. 2012 Dec;11(12):1741-57. doi: 10.1074/mcp.M112.019919. Epub 2012 Sep 10.
4
Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors.广泛存在生长因子驱动的抗癌症激酶抑制剂耐药性的潜力。
Nature. 2012 Jul 26;487(7408):505-9. doi: 10.1038/nature11249.
5
Targeting p90 ribosomal S6 kinase eliminates tumor-initiating cells by inactivating Y-box binding protein-1 in triple-negative breast cancers.靶向 p90 核糖体 S6 激酶通过使三阴性乳腺癌中的 Y 盒结合蛋白-1 失活来消除肿瘤起始细胞。
Stem Cells. 2012 Jul;30(7):1338-48. doi: 10.1002/stem.1128.
6
Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response.靶向 FOXO1/KLF6 轴调节 EGFR 信号和治疗反应。
J Clin Invest. 2012 Jul;122(7):2637-51. doi: 10.1172/JCI62058. Epub 2012 Jun 1.
7
Essential gene profiles in breast, pancreatic, and ovarian cancer cells.乳腺癌、胰腺癌和卵巢癌细胞的必需基因谱。
Cancer Discov. 2012 Feb;2(2):172-189. doi: 10.1158/2159-8290.CD-11-0224. Epub 2011 Dec 29.
8
Anti-apoptotic MCL-1 localizes to the mitochondrial matrix and couples mitochondrial fusion to respiration.抗凋亡蛋白 MCL-1 定位于线粒体基质,并将线粒体融合与呼吸耦联。
Nat Cell Biol. 2012 Apr 29;14(6):575-83. doi: 10.1038/ncb2488.
9
Regulation and function of the RSK family of protein kinases.RSK 家族蛋白激酶的调节和功能。
Biochem J. 2012 Jan 15;441(2):553-69. doi: 10.1042/BJ20110289.
10
Targeting Bcl-2 in Herceptin-Resistant Breast Cancer Cell Lines.靶向赫赛汀耐药乳腺癌细胞系中的Bcl-2
Curr Pharmacogenomics Person Med. 2011 Sep;9(3):184-190. doi: 10.2174/187569211796957584.

人表皮生长因子受体2阳性乳腺癌细胞的存活:受体信号传导至凋亡控制中心。

Survival of HER2-Positive Breast Cancer Cells: Receptor Signaling to Apoptotic Control Centers.

作者信息

Fink Marc Y, Chipuk Jerry E

机构信息

Department of Biomedical Sciences, Long Island University Post, Brookville, NY, USA.

出版信息

Genes Cancer. 2013 May;4(5-6):187-95. doi: 10.1177/1947601913488598.

DOI:10.1177/1947601913488598
PMID:24069506
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3782004/
Abstract

HER2 is overexpressed in a subset of breast cancers and controls an oncogenic signaling network that inhibits tumor cell death through the specific biochemical regulation of apoptotic pathways. In particular, the mitochondrial pathway for apoptosis is important for death induced by inhibitors of HER2. This review focuses on the connections between this oncogenic signaling network and individual components of the mitochondrial pathway. A comprehensive view of this signaling network is crucial for developing novel drugs in this area and to gain an understanding of how these regulatory interactions are altered in drug-refractory cancers.

摘要

HER2在一部分乳腺癌中过度表达,并控制着一个致癌信号网络,该网络通过对凋亡途径的特定生化调节来抑制肿瘤细胞死亡。特别是,凋亡的线粒体途径对于HER2抑制剂诱导的细胞死亡很重要。本综述聚焦于这个致癌信号网络与线粒体途径各个组分之间的联系。全面了解这个信号网络对于开发该领域的新药以及理解这些调节相互作用在耐药性癌症中是如何改变的至关重要。