[Research Progress of the Role of EMT in EGFR-TKIs Resistance of Non-small Cell Lung Cancer]

Zhongguo Fei Ai Za Zhi. 2018 Dec 20;21(12):907-911. doi: 10.3779/j.issn.1009-3419.2018.12.08.
[Article in Chinese]

Abstract

Lung cancer is the one of the malignant tumor of the highest morbidity and mortality over the world, and non-small cell lung cancer (NSCLC) makes up about 80%. Nowadays, molecular targeted therapy has been the first-line treatment for NSCLC. Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are increasingly used in the clinical treatment, but the EGFR-TKIs acquired resistance becomes the bottleneck of continuation of EGFR-TKIs therapy. Epithelial-mesenchymal transition (EMT) is a biological phenomenon in which epithelial cells are transformed into mesenchymal cells. EMT promoted metastasis, invasion of lung cancer and conferred characteristic of stem cell on cancer cells. Meanwhile, EMT is one of an important cause of EGFR-TKIs resistance in NSCLC. The recent studies have found that resistant cells restored the sensitivity to EGFR-TKIs by reversing EMT which suggested that the target of EMT may contribute to inhibit or even reverse the resistance of EGFR-TKIs. Here we make a review about research progress of EMT in EGFR-TKIs resistance in NSCLC. .

【中文题目:上皮间质转化在非小细胞肺癌EGFR-TKIs 耐药中的研究进展】 【中文摘要:肺癌是全世界范围内发病率和死亡率最高的恶性肿瘤之一,其中大约80%是非小细胞肺癌(non-small cell lung cancer, NSCLC)。目前分子靶向治疗已成为NSCLC的一线治疗方法,其中表皮生长因子受体-酪氨酸激酶抑制剂(epidermal growth factor receptor-tyrosine kinase inhibitors, EGFR-TKIs)越来越多地应用于临床治疗,但EGFR-TKI的获得性耐药成为制约EGFR-TKI继续使用的瓶颈。上皮间质转化(epithelial-mesenchymal transition, EMT)是上皮细胞转化为间质表型细胞的生物学现象,可促进肺癌转移、侵袭以及肿瘤细胞获得干性。此外,EMT也是引起NSCLC对EGFR-TKIs耐药的原因之一。有研究发现,逆转NSCLC细胞的间质表型,耐药的细胞能恢复对吉非替尼的敏感性,提示靶向EMT的治疗,或能阻止甚至是逆转NSCLC细胞对EGFR-TKIs的耐药,本文对EMT在NSCLC EGFR-TKIs耐药中的研究进展作一综述。 】 【中文关键词:肺肿瘤;EGFR-TKIs耐药;上皮间质转化;调控机制】.

Keywords: EGFR-TKIs resistance; Epithelial-mesenchymal transition; Lung neoplasms; Regulatory mechanism.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / administration & dosage*
  • Carcinoma, Non-Small-Cell Lung / drug therapy
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / physiopathology*
  • Drug Resistance, Neoplasm*
  • Epithelial-Mesenchymal Transition / drug effects*
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • Humans
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / physiopathology*
  • Protein Kinase Inhibitors / administration & dosage*

Substances

  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • EGFR protein, human
  • ErbB Receptors

Grants and funding

本文受国家重点研发计划(No.2017YFC0113500)、浙江省重大科技专项计划项目(No.2014C03032)、浙江省中医药科技计划重点研究项目(No.2015ZZ007)、吴阶平医学基金会临床科研专项资助基金(No.320.6750.14300)、“十三五”浙江省中医药(中西医结合)重点学科——肺癌创新性中西医结合诊治学(No.2017-XK-A33)资助