人成纤维细胞生长因子类似表达基因和成纤维细胞生长因子2在上皮性卵巢肿瘤组织中的表达

目的 探讨人成纤维细胞生长因子类似表达基因(hSef)和成纤维细胞生长因子2(FGF-2)在上皮性卵巢肿瘤组织中的表达及二者的关系.方法 采用免疫组化SP法检测31例卵巢恶性上皮性肿瘤(卵巢癌组)、18例卵巢良性上皮性肿瘤(良性组)和10例正常卵巢组织(正常组)中hSef和FGF-2蛋白的表达.采用逆转录聚合酶链反应(RT-PCR)检测卵巢癌组、良性组和正常组各24例组织中hSef和FGF-2 mRNA的表达水平.结果 与良性组、正常组相比,卵巢癌组hSef蛋白呈低表达(P＜0.001),而FGF-2蛋白呈高表达(P=0.002).hSef蛋白与FGF-2蛋白的表达呈负相关(rs=-0.324,P=0.012).hSefmRNA在正常组、良性组、卵巢癌组的表达呈下降趋势,而FGF-2mRNA表达呈增高趋势(P ＜0.001).hSef mRNA和FGF-2 mRNA的表达呈负相关(正常组rs=-0.910,P＜0.001;良性组rs=-0.859,P＜0.001;卵巢癌组rs=-0.888,P＜0.001).结论 在卵巢癌组织中,hSef表达下降,FGF-2表达增强.hSef的低表达减弱了FGF-2对细胞的增殖作用,促进了卵巢肿瘤的发生与发展.

Expression of hSef and FGF-2 in epithelial ovarian tumor

Objective To detect the expression of human similar expression to FGF gene(hSef)and fibroblast growth factor-2(FGF-2)and their correlation with epithelial ovarian tumor.Methods Immunohistochemical SP staining was used to detect the expression of hSef and FGF-2 proteins in 31 cases of epithelial ovarian carcinoma(EOC),18 cases of benign epithelial tumor(BET),10 cases of normal ovarian (NO)tissues collected from July 2007 to May 2008.The expression of hSef mRNA in 24 cases of EOC,BET and NO collected from July 2008 to May 2009 were analyzed by RT-PCR.Results The results of immunohistochemical study showed that the expression of hSef in the EOC tissues were significantly lower than that in the NO and BET(P ＜ 0.001).However,the expression of FGF-2 was higher(P=0.002).The expression of hSef had a negative correlation with FGF-2(rs=-0.324,P=0.012).The RT-PCR results showed that there was a gradually declined trend of expression of hSef in NO,BET to EOC(P ＜0.001),but the expression of FGF-2 in NO,BET to EOC was gradually increased(P ＜ 0.001),with a significant negative correlation(NO:rs=-0.910,P ＜ 0.001 ; BET:rs=-0.859,P ＜ 0.001 ; EOC:rs=-0.888,P ＜ 0.001).Conclusions The expression of hSef is decreased in epithelial ovarian carcinoma tissue,but the expression of FGF-2 is increased.It is likely that low hSef expression is related to the the carcinogenesis and development of epithelial ovarian carcinoma by suppressing the promoting effects of FGF-2 to cell proliferation.