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[非小细胞肺癌中微小RNA与表皮生长因子受体酪氨酸激酶抑制剂继发耐药的研究进展]

[Advance in microRNAs and EGFR-TKIs secondary resistance research in non-small cell lung cancer].

作者信息

Duan Xiaoyang, Shi Jian

机构信息

Graduate Student of Hebei Medical University, Shijiazhuang 050000, China.

Department of Medical Oncology, 
Hebei Province Cancer Hospital, Shijiazhuang 050000, China.

出版信息

Zhongguo Fei Ai Za Zhi. 2014 Dec;17(12):860-4. doi: 10.3779/j.issn.1009-3419.2014.12.07.

DOI:10.3779/j.issn.1009-3419.2014.12.07
PMID:25539612
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6000411/
Abstract

In recent years, in non-small cell lung cancer (NSCLC) targeted therapy, especially in patients with epidermal growth factor receptor (EGFR) mutations, EGFR-tyrosine kinase inhibitors (TKI) more and more come into the clinical treatment, but EGFR-TKI resistance not only influence the drug sensitivity, appear even disease progression, become the main bottleneck of its curative effect. MicroRNAs (miRNAs) is a non coding RNA and protein involved in regulating gene expression in the transcription level. Recent studies found that miRNAs involved in EGFR-TKIs resistance, which affect the sensitivity of tumor cells to treatment. In this paper, we reviewed briefly advance in miRNAs and EGFR-TKIs secondary resistance research in NSCLC.

摘要

近年来,在非小细胞肺癌(NSCLC)的靶向治疗中,尤其是在表皮生长因子受体(EGFR)突变的患者中,EGFR酪氨酸激酶抑制剂(TKI)越来越多地进入临床治疗,但EGFR-TKI耐药不仅影响药物敏感性,甚至出现疾病进展,成为其疗效的主要瓶颈。微小RNA(miRNAs)是一种参与转录水平基因表达调控的非编码RNA。最近的研究发现,miRNAs参与了EGFR-TKIs耐药,影响肿瘤细胞对治疗的敏感性。本文简要综述了NSCLC中miRNAs与EGFR-TKIs继发性耐药研究的进展。

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[Advance in microRNAs and EGFR-TKIs secondary resistance research in non-small cell lung cancer].[非小细胞肺癌中微小RNA与表皮生长因子受体酪氨酸激酶抑制剂继发耐药的研究进展]
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本文引用的文献

1
microRNA-128 plays a critical role in human non-small cell lung cancer tumourigenesis, angiogenesis and lymphangiogenesis by directly targeting vascular endothelial growth factor-C.微小RNA-128通过直接靶向血管内皮生长因子-C,在人类非小细胞肺癌的肿瘤发生、血管生成和淋巴管生成中发挥关键作用。
Eur J Cancer. 2014 Sep;50(13):2336-50. doi: 10.1016/j.ejca.2014.06.005. Epub 2014 Jul 4.
2
CRKL amplification is rare as a mechanism for acquired resistance to kinase inhibitors in lung cancers with epidermal growth factor receptor mutation.在具有表皮生长因子受体突变的肺癌中,CRKL扩增作为对激酶抑制剂获得性耐药的一种机制较为罕见。
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miR-138-5p reverses gefitinib resistance in non-small cell lung cancer cells via negatively regulating G protein-coupled receptor 124.miR-138-5p 通过负向调控 G 蛋白偶联受体 124 逆转非小细胞肺癌细胞对吉非替尼的耐药性。
Biochem Biophys Res Commun. 2014 Mar 28;446(1):179-86. doi: 10.1016/j.bbrc.2014.02.073. Epub 2014 Feb 28.
4
The insulin-like growth factor 1 receptor causes acquired resistance to erlotinib in lung cancer cells with the wild-type epidermal growth factor receptor.胰岛素样生长因子1受体在具有野生型表皮生长因子受体的肺癌细胞中导致对厄洛替尼产生获得性耐药。
Int J Cancer. 2014 Aug 15;135(4):1002-6. doi: 10.1002/ijc.28737. Epub 2014 Feb 4.
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MiR-21 overexpression is associated with acquired resistance of EGFR-TKI in non-small cell lung cancer.miR-21 过表达与非小细胞肺癌中 EGFR-TKI 的获得性耐药相关。
Lung Cancer. 2014 Feb;83(2):146-53. doi: 10.1016/j.lungcan.2013.11.003. Epub 2013 Nov 13.
6
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Mol Cancer Ther. 2014 Feb;13(2):444-53. doi: 10.1158/1535-7163.MCT-13-0448. Epub 2013 Nov 20.
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Inhibition of Hedgehog signaling sensitizes NSCLC cells to standard therapies through modulation of EMT-regulating miRNAs.抑制 Hedgehog 信号通过调节 EMT 调节 miRNA 使 NSCLC 细胞对标准治疗敏感。
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Cancer statistics for African Americans, 2013.美国非洲裔癌症统计数据,2013 年。
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MicroRNA-214 regulates the acquired resistance to gefitinib via the PTEN/AKT pathway in EGFR-mutant cell lines.微小RNA-214通过PTEN/AKT途径调节表皮生长因子受体(EGFR)突变细胞系对吉非替尼的获得性耐药。
Asian Pac J Cancer Prev. 2012;13(1):255-60. doi: 10.7314/apjcp.2012.13.1.255.