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Axl受体酪氨酸激酶在非小细胞肺癌中的作用

Function of Axl receptor tyrosine kinase in non-small cell lung cancer.

作者信息

Zhang Guoan, Wang Meng, Zhao Hongli, Cui Wen

机构信息

Cancer Pathology Research Institute, Jining Medical University, Jining, Shandong 272067, P.R. China.

Department of Oncology, Shandong Jining First People's Hospital, Jining, Shandong 272111, P.R. China.

出版信息

Oncol Lett. 2018 Mar;15(3):2726-2734. doi: 10.3892/ol.2017.7694. Epub 2017 Dec 27.

DOI:10.3892/ol.2017.7694
PMID:29434997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5778882/
Abstract

Axl receptor tyrosine kinase (hereafter Axl) is a member of the tyrosine-protein kinase receptor Tyro3, Axl and proto-oncogene tyrosine-protein kinase Mer family of receptor tyrosine kinases, possessing multiple different functions in normal cells. Axl is overexpressed and activated in numerous different human cancer types, triggering several signaling pathways and enhancing tumor progression. The present review assesses previous studies on the function of Axl in non-small cell lung cancer (NSCLC). Axl is overexpressed in the tumor tissues of a number of patients with NSCLC and is associated with poorer clinical outcomes; it promotes NSCLC tumor growth, invasion/metastasis, drug resistance and the epithelial-mesenchymal transition, thus providing a survival advantage to tumor cells. Therefore, Axl may be a promising target in NSCLC treatment.

摘要

Axl受体酪氨酸激酶(以下简称Axl)是酪氨酸蛋白激酶受体Tyro3、Axl和原癌基因酪氨酸蛋白激酶Mer家族的成员,在正常细胞中具有多种不同功能。Axl在多种不同类型的人类癌症中过度表达并被激活,触发多种信号通路并促进肿瘤进展。本综述评估了先前关于Axl在非小细胞肺癌(NSCLC)中功能的研究。Axl在许多NSCLC患者的肿瘤组织中过度表达,并与较差的临床结果相关;它促进NSCLC肿瘤生长、侵袭/转移、耐药性和上皮-间质转化,从而为肿瘤细胞提供生存优势。因此,Axl可能是NSCLC治疗中一个有前景的靶点。

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1
Function of Axl receptor tyrosine kinase in non-small cell lung cancer.Axl受体酪氨酸激酶在非小细胞肺癌中的作用
Oncol Lett. 2018 Mar;15(3):2726-2734. doi: 10.3892/ol.2017.7694. Epub 2017 Dec 27.
2
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3
AXL receptor tyrosine kinase as a therapeutic target in NSCLC.AXL受体酪氨酸激酶作为非小细胞肺癌的治疗靶点
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6
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本文引用的文献

1
AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity.AXL受体酪氨酸激酶是T细胞启动和抗病毒免疫所必需的。
Elife. 2016 Jun 28;5:e12414. doi: 10.7554/eLife.12414.
2
Axl Receptor Axis: A New Therapeutic Target in Lung Cancer.Axl受体轴:肺癌中的一个新治疗靶点。
J Thorac Oncol. 2016 Aug;11(8):1357-1362. doi: 10.1016/j.jtho.2016.04.015. Epub 2016 Apr 26.
3
Insights into the roles of hnRNP A2/B1 and AXL in non-small cell lung cancer.对异质性核糖核蛋白A2/B1和AXL在非小细胞肺癌中作用的见解。
Oncol Lett. 2015 Sep;10(3):1677-1685. doi: 10.3892/ol.2015.3457. Epub 2015 Jul 3.
4
Epithelial-to-mesenchymal transition is not required for lung metastasis but contributes to chemoresistance.上皮-间质转化并非肺转移所必需,但会导致化疗耐药。
Nature. 2015 Nov 26;527(7579):472-6. doi: 10.1038/nature15748. Epub 2015 Nov 11.
5
Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer.上皮-间质转化对胰腺癌转移并非必需,但可诱导其产生化疗耐药性。
Nature. 2015 Nov 26;527(7579):525-530. doi: 10.1038/nature16064. Epub 2015 Nov 11.
6
AXL Inhibitors in Cancer: A Medicinal Chemistry Perspective.AXL 抑制剂在癌症治疗中的应用:从药物化学角度看
J Med Chem. 2016 Apr 28;59(8):3593-608. doi: 10.1021/acs.jmedchem.5b01273. Epub 2015 Nov 20.
7
Coexpression of receptor tyrosine kinase AXL and EGFR in human primary lung adenocarcinomas.受体酪氨酸激酶AXL与表皮生长因子受体(EGFR)在人原发性肺腺癌中的共表达
Hum Pathol. 2015 Dec;46(12):1935-44. doi: 10.1016/j.humpath.2015.08.014. Epub 2015 Sep 15.
8
Kinome-wide shRNA screen identifies the receptor tyrosine kinase AXL as a key regulator for mesenchymal glioblastoma stem-like cells.全激酶组 shRNA 筛选发现受体酪氨酸激酶 AXL 是间质型神经胶质瘤干细胞样细胞的关键调节因子。
Stem Cell Reports. 2015 May 12;4(5):899-913. doi: 10.1016/j.stemcr.2015.03.005. Epub 2015 Apr 23.
9
AXL mediates resistance to PI3Kα inhibition by activating the EGFR/PKC/mTOR axis in head and neck and esophageal squamous cell carcinomas.AXL通过激活头颈部和食管鳞状细胞癌中的EGFR/PKC/mTOR轴介导对PI3Kα抑制的抗性。
Cancer Cell. 2015 Apr 13;27(4):533-46. doi: 10.1016/j.ccell.2015.03.010.
10
AUY922 effectively overcomes MET- and AXL-mediated resistance to EGFR-TKI in lung cancer cells.AUY922有效克服了肺癌细胞中MET和AXL介导的对表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)的耐药性。
PLoS One. 2015 Mar 17;10(3):e0119832. doi: 10.1371/journal.pone.0119832. eCollection 2015.