人类脱嘌呤/脱嘧啶核酸内切酶1在三阴性乳腺癌中的表达研究

目的 检测人类脱嘌呤/脱嘧啶核酸内切酶1(apurinic/apyrimidinic endonuclease/redox effector factor1,APE-1/REF-1)在乳腺癌中的表达,分析其与乳腺癌的临床病理特征的关系,及APE-1对三阴性乳腺癌患者预后的影响。方法 采用免疫组化Envision两步法检测323例乳腺癌中APE-1蛋白的表达,其中108例为三阴性乳腺癌。计数资料采用χ²检验和Fisher精确检验。采用Kaplan-Meier法进行生存分析及Log-rank检验进行生存率的比较,并用COX比例风险回归模型进行多因素分析。结果 APE-1在乳腺癌组织较癌旁组织有更高的表达,且在非三阴性乳腺癌中与肿瘤大小、腋窝淋巴结状态、临床分期、雌激素受体、人类表皮生长因子2型受体的表达显著相关(P<0.05)。在三阴性乳腺癌中,APE-1表达与肿瘤大小(P=0.006)呈正相关,且APE-1低表达组有较好的生存率(P=0.007)。腋窝淋巴结阳性的三阴性乳腺癌患者中,APE-1低表达组有较好的预后(P=0.042)。结论 APE-1是影响三阴性乳腺癌患者预后的独立因子,可能成为三阴性乳腺癌的潜在治疗靶点。

Expression of APE-1 in Triple Negative Breast Cancer

Objective To investigate the expression of Apurinic/apyrimidinic endonuclease 1 (Apurinic/apyrimidinic endonuclease/redox effector factor 1, APE-1/REF-1) in breast cancer. We analyzed the relationship between APE-1 and clinicopathological factors in breast cancer and investigate the prognostic value of APE-1 in triple negative breast cancer (TNBC) patients. Methods Immunohistochemistry with two-step Envision system was used to detect the APE-1 expression in 323 cases of breast cancer, including 108 cases of TNBC. Data were analyzed by chi-square test and Fisher''s exact test. Kaplan-Meier survival analysis method and the Log-rank test were undertaken in survival and COX proportional hazards regression model was used for multivariate analysis. Results Over-expression of APE-1 was found in breast cancer tissue compared with adjacent tissues. In non-triple-negative breast cancer, APE-1 was correlated to tumor size, axillary lymph node metastasis, clinical stage, estrogen receptor (ER), and human epidermal growth factor receptor-2(HER-2)(P<0.05). In triple-negative breast cancer, the expression of APE-1 were positively correlated with tumor size (P=0.006) and the patients with low expression of APE-1 (P=0.007) have better survival rate. In axillary lymph node metastasis patients of TNBC, low expression of APE-1 group (P=0.042) had a better prognosis. Conclusion APE-1 is an independent prognostic factor in TNBC and it could become a new potential therapeutic target of TNBC.