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目的:探讨Ephrin A1在宫颈癌中的表达意义及其与宫颈癌缺氧微环境、血管形成的关系。方法:采用免疫组织化学SP法检测65例宫颈癌组织、73例宫颈上皮内瘤样变组织和49例正常宫颈组织中Ephrin A1、EphA1受体、缺氧诱导因子-1α(HIF-1α)蛋白的表达及微血管密度(MVD),并分析宫颈癌临床病理参数和缺氧状态间的关系。结果:Eph A1在宫颈各种组织中的阳性表达率无显著性差异(P>0.05),而宫颈上皮内瘤样变、宫颈癌组织中Ephrin A1的表达明显高于正常宫颈(P<0.05),但Ephrin A1的表达在宫颈上皮内瘤样变、宫颈癌组织中无明显差异(P>0.05)。且Ephrin A1的表达与宫颈癌临床分期呈正相关(P<0.05),与组织学类型、淋巴结转移、病理分级及年龄无关(P>0.05)。在宫颈癌组织中,Eph A1的表达与HIF-1α的表达及MVD无关(r=-0.152、P=0.227,r=0.061,P=0.628),而Ephrin A1与HIF-1α的表达及MVD正相关(r=0.487,P=0.000;r=0.541,P=0.000)。结论:Eph A1在宫颈组织中的表达是稳定的,而宫颈癌发生过程中HIF-1α的高表达可能是通过刺激Ephrin A1表达而促进宫颈癌的血管形成。
Objective: To investigate the significance of Ephrin A1 expression in cervical cancer and its relationship with hypoxia microenvironment and angiogenesis in cervical cancer. Methods: The expressions of Ephrin A1, EphA1 receptor, hypoxia inducible factor-1α (HIF-1α) protein in 65 cases of cervical cancer, 73 cases of cervical intraepithelial neoplasia and 49 cases of normal cervical tissue were detected by immunohistochemical SP method (MVD), and to analyze the relationship between clinicopathological parameters and hypoxia in cervical cancer. Results: There was no significant difference in the expression of Eph A1 between various tissues of cervix (P> 0.05). However, the expression of Ephrin A1 in cervical intraepithelial neoplasia and cervical cancer was significantly higher than that in normal cervix (P <0.05) , But the expression of Ephrin A1 was not significantly different between cervical intraepithelial neoplasia and cervical cancer (P> 0.05). The expression of Ephrin A1 was positively correlated with clinical stage of cervical cancer (P <0.05), but not with histological type, lymph node metastasis, pathological grade and age (P> 0.05). In cervical cancer, the expression of Eph A1 was not related to the expression of HIF-1α and MVD (r = -0.152, P = 0.227, r = 0.061, P = 0.628) (R = 0.487, P = 0.000; r = 0.541, P = 0.000). CONCLUSION: The expression of Eph A1 is stable in cervical tissues. However, the high expression of HIF-1α in cervical carcinogenesis may promote the formation of cervical cancer by stimulating the expression of Ephrin A1.