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目的探讨FAK及EphA2在人脑胶质瘤不同病理级别中的表达,并阐述FAK及EphA2与胶质瘤发生、进展的关系。方法收集广州医学院第二医院65例人脑胶质瘤标本其中I-II级(低级恶性组)38例,Ⅲ-Ⅳ级(高度恶性组)27例,男性34例,女性31例,年龄4～72岁;肿瘤直径>5cm 30例,肿瘤直径≤5cm 35例,所有胶质瘤标本均为第一次手术切除,术前均未行放、化疗;另取14例正常新鲜脑组织做对照组。应用免疫组化sp(链霉印白素-过氧化物酶法)测定FAK和EphA2蛋白表达水平并分析其相关性。结果在人正常脑组织中未见EphA2蛋白表达,其在人脑胶质瘤高度恶性组中的表达显著高于低度恶性组(P<0.05);FAK蛋白在人正常脑组织中和脑胶质瘤中均可表达;且在人脑胶质瘤高、低度恶性组中的表达均显著高于正常脑组织(P<0.05);FAK蛋白在人脑胶质瘤高度恶性组表达显著高于低度恶性组(P<0.05)。结论 FAK及EphA2与人脑胶质瘤恶性度有关,随着恶性度增高,FAK及EphA2的表达也增加。笔者认为FAK及EphA2的高表达与胶质瘤的发生及其侵袭性生物学有关,因此FAK及EphA2可以作为胶质瘤侵袭性的生物学指标。同时以FAK及EphA2为中心的靶向治疗,可能成为抑制胶质瘤的有潜力的途径之一。
Objective To investigate the expression of FAK and EphA2 in different pathological grades of human gliomas and to elucidate the relationship between FAK, EphA2 and the occurrence and progression of gliomas. Methods Thirty-eight cases of grade I-II (low grade malignant group), 27 grade Ⅲ-Ⅳ grade (high grade group), 34 males and 31 females were collected from 65 cases of glioma in the second hospital of Guangzhou Medical College. 4 ~ 72 years old; tumor diameter> 5cm in 30 cases, tumor diameter ≤ 5cm 35 cases, all the glioma specimens were the first surgical resection, preoperative radiotherapy and chemotherapy were not performed; the other 14 cases of normal fresh brain tissue do Control group. Immunohistochemical SP (streptavidin-peroxidase method) FAK and EphA2 protein expression levels were analyzed and analyzed. Results No expression of EphA2 protein was found in normal human brain. The expression of EphA2 protein in human malignant glioma group was significantly higher than that in low grade malignant glioma group (P <0.05) The expression of FAK protein in human glioma was significantly higher than that in normal brain tissue (P <0.05). The expression of FAK protein in human glioma group was significantly higher than that in normal brain glioma In the low-grade group (P <0.05). Conclusions FAK and EphA2 are associated with the degree of malignancy of human glioma. The expression of FAK and EphA2 also increased with the increase of malignancy. I believe that the high expression of FAK and EphA2 and the occurrence of glioma and invasive biology, so FAK and EphA2 can be used as biological indicators of invasive glioma. At the same time, targeted therapy with FAK and EphA2 may be one of the potential ways to inhibit gliomas.