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目的探讨粘着斑激酶(focal adhesion kinase,FAK)介导血管内皮细胞生长因子C(vascularendothelial growth factor C,VEGF-C)促宫颈癌恶性进展的作用。方法提取不同病理分期的宫颈癌组织标本蛋白,采用Western-blot检测VEGF-C及FAK蛋白的表达情况。在体外培养宫颈癌细胞株HeLa细胞,采用Western-blot测定VEGF-C对FAK蛋白的表达和磷酸化的调控作用。结果随着宫颈癌恶性程度的增高,VEGF-C、FAK蛋白及磷酸化FAK蛋白表达水平均随之增加。与正常宫颈组织比较,宫颈原位癌(CIN)组织中VEGF-C、FAK、磷酸化FAK蛋白表达分别增加了(48±10)%、(78±14)%、(83±15)%,P<0.05;宫颈鳞癌Ⅰ期各蛋白增高幅度分别为(104±22)%、(121±28)%、(143±30)%(P<0.01);宫颈鳞癌Ⅱ期(未放疗、化疔)各蛋白表达增高更为显著,其幅度分别为(195±28)%、(186±22)%、(204±31)%,P<0.001。在培养的宫颈癌细胞株HeLa细胞上,VEGF-C(100μg/L)处理24 h后,可显著增高FAK蛋白、磷酸化FAK蛋白的表达,该作用可被VEGF-C单克隆抗体明显抑制。结论 VEGF-C、FAK蛋白表达与宫颈癌恶性程度密切相关,VEGF-C可能通过上调FAK表达及其磷酸化水平而促进宫颈癌的恶性进展。
Objective To investigate the role of focal adhesion kinase (FAK) in the malignant progression of cervical carcinoma mediated by vascular endothelial growth factor C (VEGF-C). Methods Cervical cancer tissue samples of different pathological stages were extracted, and the expression of VEGF-C and FAK protein was detected by Western-blot. The cervical cancer cell line HeLa was cultured in vitro, and the effect of VEGF-C on FAK protein expression and phosphorylation was determined by Western-blot. Results With the increase of malignant degree of cervical cancer, the expressions of VEGF-C, FAK protein and phosphorylated FAK protein increased. Compared with normal cervical tissue, the expressions of VEGF-C, FAK and phosphorylated FAK in cervical intraepithelial carcinoma (CIN) increased by 48 ± 10%, 78 ± 14% and 83 ± 15%, respectively (104 ± 22)%, (121 ± 28)% and (143 ± 30)%, respectively (P <0.01); The positive rate of cervical squamous cell carcinoma in stage Ⅱ (without radiotherapy, (195 ± 28)%, (186 ± 22)%, (204 ± 31)%, P <0.001, respectively. After treatment with VEGF-C (100μg / L) for 24 hours on HeLa cells, the expression of FAK and phosphorylated FAK protein was significantly increased, which was significantly inhibited by VEGF-C monoclonal antibody. Conclusion The expressions of VEGF-C and FAK are closely related to the malignant degree of cervical cancer. VEGF-C may promote the malignant progression of cervical cancer by up-regulating FAK expression and phosphorylation.