中文摘要：

目的 分析磷酸化AKT（p-AKT）及其下游分子Cyclin D1、MMP-9在非小细胞肺癌（NSCLC）中的表达情况，探讨p-AKT及其下游分子在肺癌发病机制中的作用。方法 应用免疫组化的方法，检测80例NSCLC组织及35例非肿瘤性肺组织标本中P—AKT、Cyclin D1和MMP-9的表达，并与临床病理因素进行相关性分析。结果p—AKT、Cyclin D1和MMP-9在NSCLC中高表达，阳性率分别为78．8％、76．3％和72．5％，显著高于非肿瘤性肺组织中阳性表达0、0和11．4％（P〈0．05）。p-AKT在高中分化腺癌中阳性表达（95．0％）显著高于低分化腺癌的表达（50．0％）（P〈0．05），而与患者年龄、性别、组织学类型及鳞癌的分化程度、TNM分期、淋巴结转移无关（P〉0.05）。CyclinD1、MMP-9表达与淋巴结转移、鳞癌的分化程度有关（P〈0.05），MMP-9还与TNM分期有关（P〈0.05），P—AKT的表达与Cyclin D1呈正相关（rs=0．787，P〈0．01），与MMP-9蛋白表达无关（rs=0．022，P〉0.05）。结论 在NSCLC中存在AKT的活化，Cyclin D1的高表达可能与AKT的活化有关，MMP-9可能通过其他的调控机制参与了肺癌的发生发展。在NSCLC组织中存在着AKT信号转导通路的激活。

英文摘要：

[Objective] To investigate the expression of phospho-AKT （p-AKT） and its target gene products including Cyelin D1 and MMP-9 in human non-small cell lung cancer （NSCLC） tissue, and to explore the mechanisms in tumorgenesis of NSCLC. [Methods] The expression of p-AKT, Cyelin D1, MMP-9 in 80 cases of NSCLC and 35 cases of no-cancerous lung disease were assessed by immunohistoehemistry, and their correlations with eliniopathological factors were statistically analyzed. [Results] The positive rate of p-AKT, Cyelin D1, MMP-9 was 78.8%, 76.3%, 72.5% in NSCLC and 0%, 0%, 11.4% （P 〈0.05） in no-cancerous lung disease. The positive rate of p-AKT in Well-differentiated and moderately-differentiated adenoeareinoma （95.0%） was significantly higher than that of p- AKT in poorly-differentiated adenoeareinoma （50.0%） （P 〈0.05）. The expression of p-AKT didn＇t relate to age, sex, histologie subtype and Squamous cancer differentiation, lymph node metastasis and TNM stages （P 〉0.05）. The expression of Cyelin D1 and MMP-9 correlated with lymph node metastasis and differentiation of squamous cell carcinoma （P 〈0.05）, The expression of MMP-9 correlated with TNM stages （P 〈0.05）. In addition, The expression of p- AKT had a positive correlation with the expression of Cyelin D1 （P 〈0.01） and no correlation with the expression of MMP-9 （P 〉0.05）. [Conclusion] AKT activation may be present in NSCLC tissues. The high positive rate of CyclinD1 may correlate to activation of AKT. MMP-9 may participate in carcinogenesis and development of lung cancer through other routes. PI3K/AKT signaling pathway is activated in NSCLC tissues.