PI3K/AKT信号通路相关蛋白在乳腺癌中的表达及其临床意义

Expression of proteins associated with PI3K/AKT signaling pathway in breast cancer and the clinical significance

目的研究PI3K/AKT信号转导通路中PTEN、PI3K、AKT蛋白在乳腺癌中的表达及其与疾病发生发展、预后的关系。方法用免疫组化SP法检测45例乳腺癌患者病理组织(观察组)和其中15例患者癌旁正常组织(对照组)中PTEN、PI3K、AKT表达情况,采用单因素回归分析对PTEN、PI3K、AKT蛋白在乳腺癌组织中阳性表达的相关因素进行分析。结果 PI3K、AKT在乳腺癌中的表达率分别为73.3%、75.5%,高于癌旁正常乳腺组织的33.3%、40%,差异具有统计学意义(P﹤0.05);PTEN在乳腺癌中表达率为22.2%,低于癌旁正常乳腺组织的53.3%,但差异无统计学意义(P﹥0.05);单因素回归分析结果显示,患者发病年龄对PTEN、PI3K、AKT在乳腺癌组织中阳性表达无关(P﹥0.05);组织学分级、临床分期、存在淋巴结转移是PTEN、PI3K、AKT在乳腺癌组织中的阳性表达的相关因素(P﹤0.05)。结论 PI3K/AKT信号通路可能参与了乳腺癌的发生与发展,PTEN蛋白表达缺失导致AKT、PI3K蛋白的过度表达,PI3K、PTEN、AKT蛋白表达的检测可能有助于预测乳腺癌的预后。

Objective To investigate the expressions of PTEN, PI3K, and AKT in breast cancer and their relevance with the occurrence, development and prognosis of breast cancer. Method The expression of PTEN, PI3K and AKT in 45 cases of breast cancer （observer group） and 15 cases with normal adjacent tissues （comparison group） were determined using SP method of immunohistochemistry, and univariate analysis was applied to analyze the factors related with posi-tive expression of PTEN, PI3K, and AKT protein in breast cancer tissues. Result The PI3K and AKT expression rate in breast cancer was 73.3%and 75.5%, higher than that in normal adjacent tissues at 33.3%and 40%, respectively （P〈0.05）;the expression rate of PTEN in breast cancer was 22.2%, lower than that of the adjacent normal tissues at 53.3%, and no significant difference was observed （P〉0.05）;the univariate analysis showed that, age was irrelevant （P〉0.05）;while his-tological grade, clinical stage, axillary lymph node metastasis were factors associated with positive expression of PTEN, PI3K, and AKT in breast cancer tissues （P〈0.05）. Conclusion PI3K/AKT signaling pathway may be involved in the oc-currence and development of breast cancer, and the loss of expression of PTEN may contribute to overexpression of PI3K and AKT in breast cancer, so the detection of PTEN, PI3K and AKT may be helpful to predict the prognosis of breast can-cer.