Huang Jun, He Yujiao, Chen Mingna, Du Juan, Li Guoliang, Li Shuyu, Liu Weiping, Long Xiaoyan
Department of Neurosurgery, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
Department of Neurology, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
Mol Med Rep. 2015 Nov;12(5):6509-16. doi: 10.3892/mmr.2015.4285. Epub 2015 Sep 2.
The aim of the present study was to investigate adenosine deaminase (ADA) and adenosine kinase (ADK) expression in human glioma and to explore its correlation with glioma‑associated epilepsy. Tumor tissues (n=45) and peritumoral tissues (n=14) were obtained from glioma patients undergoing surgery. Normal control tissues (n=8) were obtained from brain trauma patients. The disease grade was determined by histological evaluation and the degree of tumor invasion was evaluated using immunofluorescence analyses. mRNA and protein expression of ADA and ADK were evaluated using reverse transcription quantitative polymerase chain reaction or western blot analysis, respectively. Based on histological evaluations, four cases were classified as Grade I gliomas, 18 cases as Grade II, 17 cases as Grade III and six cases were considered Grade IV. Increased ADA and ADK expression was observed in tumor tissues. ADA was predominantly distributed in the cytoplasm of tumor cells, whereas ADK was detected in the cytoplasm as well as in the nuclei. ADA and ADK levels were upregulated in patients with Grade II and Grade III gliomas compared to those in control subjects (p<0.05). In addition, tumor invasion was detected in peritumoral tissues. The number of ADA‑positive or ADK‑positive cells in tumor tissues was similar between glioma patients with and without epilepsy (p>0.05). However, ADA and ADK expression was upregulated in peritumoral tissues derived from patients with epilepsy compared to that in glioma patients without epilepsy. The results of the present study suggested that ADA and ADK are involved in glioma progression, and that increased ADA and ADK levels in peritumoral tissues may be associated with epilepsy in glioma patients.
本研究的目的是调查人胶质瘤中腺苷脱氨酶（ADA）和腺苷激酶（ADK）的表达，并探讨其与胶质瘤相关性癫痫的关系。从接受手术的胶质瘤患者中获取肿瘤组织（n = 45）和瘤周组织（n = 14）。从脑外伤患者中获取正常对照组织（n = 8）。通过组织学评估确定疾病分级，并使用免疫荧光分析评估肿瘤侵袭程度。分别使用逆转录定量聚合酶链反应或蛋白质印迹分析评估ADA和ADK的mRNA和蛋白质表达。根据组织学评估，4例被分类为I级胶质瘤，18例为II级，17例为III级，6例被认为是IV级。在肿瘤组织中观察到ADA和ADK表达增加。ADA主要分布在肿瘤细胞的细胞质中，而ADK在细胞质以及细胞核中均有检测到。与对照组相比，II级和III级胶质瘤患者的ADA和ADK水平上调（p<0.05）。此外，在瘤周组织中检测到肿瘤侵袭。有癫痫和无癫痫的胶质瘤患者肿瘤组织中ADA阳性或ADK阳性细胞数量相似（p>0.05）。然而，与无癫痫的胶质瘤患者相比，癫痫患者瘤周组织中的ADA和ADK表达上调。本研究结果表明，ADA和ADK参与胶质瘤进展，且瘤周组织中ADA和ADK水平升高可能与胶质瘤患者的癫痫有关。
