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出核因子CRM1及p27在胶质瘤中的表达
引用本文:王东林,王燏婵,LU Peng,鄂群,施公胜.出核因子CRM1及p27在胶质瘤中的表达[J].中华病理学杂志,2008,37(7):454-457.
作者姓名:王东林  王燏婵  LU Peng  鄂群  施公胜
作者单位:1. 江苏省南通大学医学院病理学教研室,226001
2. Department of Pathology, Medical College of Nantong University, Nantong 226001, China
3. 南通大学附属医院病理科
基金项目:江苏省高校自然科学基金 
摘    要:目的 探讨出核因子CRM1、p27 10位丝氨酸(Ser10)磷酸化及p27蛋白在胶质瘤中的表达、相互关系及意义.方法 免疫组织化学SP法检测70例胶质瘤和10例非肿瘤对照脑组织标本中CRM1、p27Ser10磷酸化形式及p27蛋白的表达,Western blot检测6例新鲜胶质瘤标本中相应蛋白的表达.结果 CRM1及p27Ser10磷酸化形式在对照脑组织中表达不明显,在低级别胶质瘤中表达较少,在高级别胶质瘤中表达较多,两两比较差异均有统计学意义(P<0.01).p27在对照脑组织中表达明显,其表达水平随肿瘤级别增高而降低,差异有统计学意义(P<0.01).Western blot结果显示CRM1、p27Ser10磷酸化形式在胶质瘤中的表达水平与肿瘤细胞的恶性程度相关.相关分析显示:胶质瘤中CRM1蛋白表达与p27蛋白表达呈负相关(r=0.727,P<0.01),与p27Ser10磷酸化形式呈正相关(rs=0.954,P<0.01),与增殖指标Ki-67表达呈正相关(rs=0.799,P<0.01);p27Ser10磷酸化形式与p27蛋白表达呈负相关(rs=-0.744,P<0.01),与Ki-67表达呈正相关(rs=0.785,P<0.01).结论 在胶质瘤中高表达的CRM1可能通过识别并结合高表达的p27Ser10磷酸化形式,促进p27的出核降解,使p27表达降低,失去对细胞周期的调控,从而促进胶质瘤的恶性进展和增殖.

关 键 词:神经胶质瘤  周期素依赖激酶抑制剂p27  出核因子

Expression of nuclear export factor CRM1 and p27 in glioma
WANG Dong-lin,WANG Yu-chan,LU Peng,E Qun,SHI Gong-sheng.Expression of nuclear export factor CRM1 and p27 in glioma[J].Chinese Journal of Pathology,2008,37(7):454-457.
Authors:WANG Dong-lin  WANG Yu-chan  LU Peng  E Qun  SHI Gong-sheng
Abstract:Objective To investigate the expression of nuclear export factor CRM1, Ser10-phosphorylated p27 and p27 in human gliomas. Methods The expression of CRM1, Ser10-phosphorylatedp27 and p27 were investigated in 70 cases of human gliomas and 10 specimens of the normal brain tissue byimmunohistochemical technique and Western blot. Results There were significant differences on theexpression levels of CRM1, Ser10-phosphorylated p27 and p27 among normal brain tissue, gliomas of gradesⅡ and gliomas of grades Ⅲ plus Ⅳ (P < 0. 01). The expression of CRM1 in gliomas was inverselycorrelated with the expression of p27 (rs =-0. 727, P < 0. 01) and positively correlated with the expressionof Ser10-phosphorylated p27 (rs = 0. 954, P < 0. 01) and Ki-67 (rs = 0. 799, P < 0. 01). Moreover, theexpression of Ser10-phosphorylated p27 was inversely correlated with p27 (rs= - 0. 744, P < 0. 01) andpositively correlated with Ki-67 (r, = 0. 785, P < 0. 01). Conclusions CRM1, through recognizing andbinding with Ser10-phosphorylated p27, may promote moving of p27CRM1 from its original locating sites;act as a critical signaling component in the proliferative process of glioma cells and then, plays an importantrole in the development of gliomas.
Keywords:Glioma  C yelin-dependent kinase inhibitor p27  Nuclear export factor
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