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目的探讨磷脂酰肌醇3激酶/蛋白激酶B1/哺乳动物雷帕霉素靶蛋白(PI3K/Akt1/m TOR)通路与表皮生长因子受体(EGFR)基因的关系,及其PI3K/Akt1/m TOR通路导致EGFR-酪氨酸激酶抑制剂(TKI)耐药的具体机制。方法选择135例未经过放化疗或靶向药物治疗的非小细胞肺癌(NSCLC)患者的肿瘤组织标本,检测其EGFR、PIK3CA、Akt1和m TOR的mRNA表达水平,并进行相关性分析。结果 EGFR与Akt1、m TOR的表达水平呈正相关(r分别为0.342、0.320和0.281,均P<0.01),与PIK3CA基因无关。结论 EGFR基因表达与Akt1和m TOR相关,与PIK3CA无关,提示EGFR基因可能直接激活Akt及其下游通路,而不经过PI3K。
Objective To investigate the relationship between the phosphoinositide 3 kinase / protein kinase B1 / mammalian target of rapamycin (PI3K / Akt1 / m TOR) pathway and the epidermal growth factor receptor (EGFR) gene and its PI3K / Akt1 / m TOR pathway leads to the specific mechanism of EGFR-tyrosine kinase inhibitor (TKI) resistance. Methods Tumor samples of 135 non-small cell lung cancer (NSCLC) patients who had not been treated with radiotherapy and chemotherapy were selected and the mRNA expression levels of EGFR, PIK3CA, Akt1 and m TOR were detected and analyzed. Results The expression of EGFR was positively correlated with Akt1 and mTOR (r = 0.342,0.320 and 0.281, all P <0.01), but not with PIK3CA. Conclusion EGFR gene expression is related to Akt1 and m TOR but not to PIK3CA, suggesting that EGFR may directly activate Akt and its downstream pathway without PI3K.