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非小细胞肺癌中microRNAs与EGFR-TKIs继发性耐药机制的研究进展 被引量:3

Advance in MicroRNAs and EGFR-TKIs Secondary Resistance Research in Non-small Cell Lung Cancer
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摘要 近年来,在非小细胞肺癌(non-small cell lung cancer,NSCLC)靶向治疗中,尤其是伴有表皮生长因子受体(epidermal growth factor receptor,EGFR)基因突变的患者,EGFR酪氨酸激酶抑制剂(tyrosine kinase inhibitor,TKI)越来越多地进入到临床治疗,但EGFR-TKI耐药的产生不仅影响药物敏感性,甚至出现疾病进展,成为制约其疗效的主要瓶颈。微小RNA(microRNAs,mi RNAs)是一种非编码蛋白的RNA,参与转录后水平基因的表达调控,最近研究发现,miRNAs参与了EGFR-TKIs耐药,影响肿瘤细胞对吉非替尼的敏感性。本文就NSCLC中mi RNAs与EGFR-TKIs继发性耐药之间的相关性研究进展做简要的综述。 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 inlfuence 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 brielfy advance in miRNAs and EGFR-TKIs secondary resis-tance research in NSCLC.
作者 段晓阳 史健
出处 《中国肺癌杂志》 CAS 北大核心 2014年第12期860-864,共5页 Chinese Journal of Lung Cancer
关键词 肺肿瘤 MICRORNAS EGFR-TKIS 继发性耐药 Lung neoplasms MicroRNAs EGFR-TKIs Secondary resistance
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  • 1DeSantis C, Naishadham D, Jemal A. Cancer statistics for African Americans, 2013. CA CancerJ Clin, 2013, 63(3): 151-166.
  • 2Jemal A, Bray F, Center MM, et al. Global cancer statistics. CA Cancer J Clin, 2011, 61(2): 69-90.
  • 3Jackman D, Pao W,, Riely G J, et al. Clinical definition of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small celt lung cancer. J Clin Oncol, 2010, 28(2): 357-360.
  • 4Pao W,, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib isassociated witha second mutation in the EGFR kinase domain. PLoS Med, 2005, 2(3): e73.
  • 5Engelman JA, Zejnullahu K, Mitsudomi T, et al. MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science, 2007, 316(5827): 1039-1043.
  • 6Uramoto H, Iwata T, Onitsuka T, et al. Epithelial-mesenchymal transition in EGFR-TKI acquired resistant lung adenocarcinoma. Anticancer Res, 2010, 30(7): 2513-2517.
  • 7Sos ML, Koker M, Weir BA, et al. PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFR. Cancer Res, 2009, 69(8): 3256-3261.
  • 8Webster RJ, Giles KM, Price KJ, et al. Regulation of epidermal growth factor receptor signaling in human cancer cells by microRNA-7. J Biol Chem, 2009, 284(9): 5731-5741.
  • 9Hurbin A, Wislez M, Busser B, et al. Insulin-like growth factor-1 receptor inhibition overcomes gefitinib resistance in mucinous lung adenocarcinoma. J Pathol, 2011, 225(1): 83-95.
  • 10Suda K, Miznuchi H, Sato K, et al. ~he insulin-like growth factor 1 receptor causes acquired resistance to edotinib in lung cancer cells with the wild-type epidermal growth factor receptor. IntJ Cancer, 2014, 135(4): 1002-1006.

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