摘要
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 explore the relationship between phosphotylinosital 3 kinase/protein kinase B 1/mammalian target of rapamycin （PI3K/Aktl/mTOR） pathway and epidermal growth factor receptor （EGFR） gene, and lay the foundation for the related mechanisms of PI3K/Aktl/mTOR pathway in EG- FR-tyrosine kinase inhibitor （TKI） resistance. Methods Detecting the mRNA expressions of PIK3CA, Aktl, mTOR and EGFR in 135 non-small cell lung cancer （NSCLC） patients without any treatment, and the correlation was analyzed. Results EGFR, Aktl and mTOR gene expressions are con＇elated with each other （r=0. 342, 0. 320 and 0.281; P〈0. 01）, other than PIK3CA gene. Conclusion EGFR gene expression is related to Aktl and mTOR other than PIK3CA, which indicate that EGFR gene may activate Aktl and its downstream directly, not through PI3K.
出处
《中国肿瘤临床与康复》
2014年第12期1409-1412,共4页
Chinese Journal of Clinical Oncology and Rehabilitation
基金
解放军总医院临床科研扶持基金
No.2014FC-TSYS-4015
