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PI3K/Akt/mTOR信号转导途径与非小细胞肺癌的关系 被引量:1

The Relationship between the PI3K/Akt/mTOR Signal Transduction Pathway and Non-Small Cell Lung Cancer
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摘要 背景与目的PI3K/Akt/mTOR通路失调对肺癌形成可能具有重要作用,本研究通过分析非小细胞肺癌组织中PI3K/Akt/mTOR信号转导途径中VEGF,PI3K,Akt,mTOR基因的表达水平,探讨PI3K/Akt/mTOR信号转导途径与非小细胞肺癌之间的关系。方法外科手术中获取40例非小细胞肺癌组织及30例癌旁组织,应用逆转录聚合酶链反应(reverse transcriptase polymerase chain reaction,RT—PCR)技术检测癌及癌旁组织中VEGF,PI3K,Akt,mTOR基因的表达水平。结果非小细胞肺癌组织中VEGF,PI3K,Akt,mTOR基因的表达水平分别为(40±59)%、(61±23)%,(77±32)%,(43±21)%,癌旁组织中VEGF,PI3K,Akt、roTOR基因的表达水平分别为(16±40)%、(23±16)%、(10±12)%、(20±17)%,非小细胞肺癌组织中VEGF、PI3K,Akt,mTOR基因的表达水平均高于癌旁组织(P〈0.01)。联合应用4个基因表达作为NSCLC诊断标志,诊断的敏感性达到87.5%,特异性为90%。结论非小细胞肺癌中PI3K/Akt/mTOR信号转导途径相关基因表达水平明显上调,说明该通路在非小细胞肺癌中被激活. 联合检测VEGF、PI3K、Akt、mTOR的表达水平改变可能作为NSCLC的诊断标志。 Background and objective It has been known that abnormality of PI3K/Akt/mTOR signal pathway played an important role in the oncogenesis of lung cancer. In this study, we tried to detect the mRNA expression levels of VEGF, PI3K, Akt, roTOR gene, the key genes of PI3K/Akt/mTOR signal pathway, in human non-small cell lung cancer (NSCLC) tissue and explore the relationship between PI3K/Akt/mTOR signaling pathway and non-small cell lung cancer. Methods Lung cancer tissue specimens were obtained from 40 patients. Adjacent-tumor NSCLC tissues from the 30 patients were served as control. The RT-PCR technique was used to detect the VEGF, PI3K, Akt, roTOR gene expression levels. Results The average mRNA expression levels of VEGF,, PI3K, Akt, roTOR gene in lung cancer were (40±59)%,(61 ± 23)%, (77±32)% and (43±21)% respectively, while the mRNA expression levels of VEGF, PI3K, Akt, mTOR genes in adjacent-tumor tissue were (16±40)%, (23±16)%, (10±12)% and (20±17)%, respectively. All the levels of VEGF, PI3K, Akt, mTOR gene expression in NSCLC were significantly higher than that in adjacent-tumor lung tissue (P〈0.01). Conclusion Our preliminary data have demonstrated that PI3K/Akt/mTOR signaling pathway is activated in the tumor cells of NSCLC. The activated PI3K/Akt/mTOR signaling pathway might be an important role in the pathogenesis of NSCLC.
出处 《结核病与胸部肿瘤》 2009年第2期92-96,共5页 Tuberculosis and Thoracic Tumor
基金 本研究受北京市科技新星(No.2006834)、教育部出国留学回国启动基金和北京市优秀人才培养基金(No.20061D03)资助
关键词 肺肿瘤 VEGF PI3K AKT MTOR Lung neoplasms Vascular endothelial growth factor A Human l-phosphatidylinositol 3-kinase p110 subunit Oncogene protein v-akt Mammalian target of rapamycin (mTOR)
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