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Overexpression of centrosomal protein 55 regulates the proliferation of glioma cell and mediates proliferation promoted by EGFRvIII in glioblastoma U251 cells

机译:中心体蛋白55的过表达调节胶质瘤细胞U251细胞中神经胶质瘤细胞的增殖并介导EGFRvIII促进的增殖

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摘要

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.
机译:表皮生长因子受体(EGFR)通常在神经胶质瘤中扩增,最常见的细胞外结构域突变是EGFR变体III(EGFRvIII)。 EGFRvIII信号异常已被证明在驱动肿瘤进展中很重要。中心体相关蛋白家族的成员中心体蛋白55(CEP55)参与细胞周期的细胞分裂。它存在于一些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。在这项研究中,在40例神经胶质瘤组织和10例非肿瘤脑组织中检测到CEP55的表达。用EGFRvIII和CEP55 siRNA转染后,分析了胶质母细胞瘤U251细胞的增殖。我们发现脑胶质瘤组织中CEP55的表达明显高于正常脑组织。用EGFRvIII转染后,U251细胞的增殖显着增加。敲低CEP55抑制U251细胞的增殖,并能消除促进EGFRvIII诱导的U251细胞增殖的作用。 CEP55在神经胶质瘤细胞的增殖和神经胶质瘤细胞介导的EGFRvIII刺激的增殖中起关键作用。 CEP55可能是表达EGFRvIII的神经胶质瘤患者的新型分子治疗靶标。

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