Zhu Hongfan, Chen Diangang, Tang Jinliang, Huang Changlin, Lv Shengqing, Wang Donglin, Li Guanghui
Institute for Cancer Research in People's Liberation Army, Xinqiao Hospital, The Third Military Medical University, P.R. China.
Department of Pathology, Xinqiao Hospital, The Third Military Medical University, P.R. China.
Oncol Lett. 2018 Feb;15(2):2700-2706. doi: 10.3892/ol.2017.7573. Epub 2017 Dec 8.
The epidermal growth factor receptor (EGFR) is often amplified in glioma, with the most common extracellular domain mutation being EGFR variant III (EGFRvIII). Abnormal EGFRvIII signaling has been shown to be important in driving tumor progression. Centrosomal protein 55 (CEP55), a member of the centrosomal relative proteins family, participates cytokinesis in the cell cycle. It exists in a few normal tissues and various tumor cells. The expression and function of CEP55 in human glioma cells need to investigate. In this study, the expression of CEP55 was detected in 40 cases of glioma tissues and 10 cases of non-tumor brain tissue. The proliferation of glioblastoma U251 cells was analyzed after transfection with EGFRvIII and CEP55 siRNA. We found that the expression of CEP55 was increased significantly in the glioma tissues than in normal brain tissue. The proliferation of U251 cells increased remarkably after transfection with EGFRvIII. Knockdown of CEP55 inhibited proliferation of U251 cells and was able to eliminate the effect of promoting proliferation induced by EGFRvIII in U251 cells. CEP55 played a key role in the proliferation of glioma cells and mediated EGFRvIII-stimulated proliferation in glioma cells. CEP55 might be a novel molecular therapeutic target in patients with gliomas expressing EGFRvIII.
表皮生长因子受体（EGFR）在胶质瘤中常发生扩增，最常见的细胞外结构域突变是EGFR变异体III（EGFRvIII）。异常的EGFRvIII信号传导已被证明在驱动肿瘤进展中起重要作用。中心体蛋白55（CEP55）是中心体相关蛋白家族的成员，参与细胞周期中的胞质分裂。它存在于少数正常组织和各种肿瘤细胞中。CEP55在人胶质瘤细胞中的表达和功能有待研究。在本研究中，检测了40例胶质瘤组织和10例非肿瘤脑组织中CEP55的表达。用EGFRvIII和CEP55 siRNA转染后分析胶质母细胞瘤U251细胞的增殖情况。我们发现，与正常脑组织相比，胶质瘤组织中CEP55的表达显著增加。用EGFRvIII转染后，U251细胞的增殖明显增加。敲低CEP55可抑制U251细胞的增殖，并能消除EGFRvIII对U251细胞增殖的促进作用。CEP55在胶质瘤细胞增殖中起关键作用，并介导EGFRvIII刺激的胶质瘤细胞增殖。CEP55可能是表达EGFRvIII的胶质瘤患者的一个新的分子治疗靶点。
