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作 者:柴春香[1] 王晓敏[2] 郭文君[2] 孙永红[2]
机构地区:[1]潍坊医学院附属医院医务科,山东潍坊261000 [2]潍坊医学院附属医院病理科,山东潍坊261000
出 处:《中国现代医学杂志》2016年第3期34-38,共5页China Journal of Modern Medicine
摘 要:目的探讨非小细胞肺癌(NSCLC)中上皮细胞间质转型(EMT)与表皮生长因子受体(EGFR)的相关性。方法免疫组织化学法(En Vision)检测78例晚期NSCLC组织和16例正常肺组织中的EGFR、E-钙黏素(E-cadherin)和波蛋白(Vimentin)的表达。EGFR 18~21号外显子聚合酶链反应(PCR)扩增及基因测序。结果78例NSCLC中,EGFR、E-cadherin和Vimentin在NSCLC中阳性表达率分别为61.5%(48/78)、43.6%(34/78)和56.4%(44/78),EGFR基因突变率为24.4%(19/78),正常组为阴性。EGFR野生型组的EMT发生率高(67.8%vs 21.1%),EGFR蛋白与EMT呈正相关性(r=0.236,P=0.037)。结论 E-cadherin降低或全部丢失及EGFR通过信号传导通路可以促进EMT的发生。Objective To investigate the relationship of epithelial-mesenchymal transition (EMT) and epi- dermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC). Methods Immunohistoehemistry (EnVision method) was used to detect the expressions of EGFR, E-cadherin and vimentin. Exons 18-21 of EGFR were detected by PCR and gene sequencing. Results The positive expression rate of EGFR, E-cad- herin and vimentin was 61.5% (48/78), 43.6% (34/78), 56.4% (44/78) respectively in the 78 cases of NSCLC; while they were not expressed in the normal group. The mutation rate of EGFR gene was 24.4% (19/78) in the NSCLC group. The incidence of EMT was higher in the EGFR wild-type group than in the mutation group (67.8% vs 21.1%). There was a positive correlation between EGFR protein expression and EMT (r= 0.236, P= 0.037). Conclusions Lost E-cadherin and EGFR signaling pathways could promote the formation of EMT.
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