Li Feng, Jin Dan, Tang Chuanxi, Gao Dianshuai
Department of Cell Biology and Neurobiology, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China.
Department of Otolaryngology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221004, P.R. China.
Oncol Lett. 2018 Apr;15(4):4789-4796. doi: 10.3892/ol.2018.7934. Epub 2018 Feb 2.
Human glioma is one of the major malignancies worldwide with an increased mortality rate. Centrosomal protein of 55 kDa (CEP55) is an essential component of the CEP family and has been identified as a prognostic marker for multiple types of cancer. However, the function of CEP55 during glioma tumorigenesis remains unclear. In the present study, the data derived from the Oncomine database indicated that the expression of CEP55 is increased in glioma tissues compared with normal tissues. Furthermore, the expression of CEP55 was also increased at the level of mRNA and protein in glioma cell lines compared with normal human astrocytes. The knockdown of CEP55 expression inhibited the proliferation of glioma U251 cells, whereas overexpression of CEP55 induced the proliferation of U251 cells. Flow cytometric analysis indicated that the knockdown of CEP55 resulted in an increased number of cells arrested at G/M phase, and apoptosis was promoted. Further investigations revealed that the overexpression of CEP55 increased the phosphorylation of Akt and inhibited the activity of p21. By contrast, the knockdown of CEP55 resulted in the opposite effects. Taken together, the results of the present study suggested that CEP55 regulated the proliferation of glioma cells, further attributing to the carcinogenesis and progression of glioma via the PI3K/Akt/p21 signaling pathway. Therefore, CEP55 may be a novel therapeutic target for the treatment of glioma.
人类胶质瘤是全球主要的恶性肿瘤之一，死亡率不断上升。55 kDa中心体蛋白（CEP55）是CEP家族的重要组成部分，已被确定为多种癌症的预后标志物。然而，CEP55在胶质瘤发生过程中的功能仍不清楚。在本研究中，来自Oncomine数据库的数据表明，与正常组织相比，胶质瘤组织中CEP55的表达增加。此外，与正常人星形胶质细胞相比，胶质瘤细胞系中CEP55在mRNA和蛋白水平的表达也增加。CEP55表达的敲低抑制了胶质瘤U251细胞的增殖，而CEP55的过表达诱导了U251细胞的增殖。流式细胞术分析表明，CEP55的敲低导致停滞在G/M期的细胞数量增加，并促进了细胞凋亡。进一步研究发现，CEP55的过表达增加了Akt的磷酸化并抑制了p21的活性。相反，CEP55的敲低则产生相反的效果。综上所述，本研究结果表明，CEP55通过PI3K/Akt/p21信号通路调节胶质瘤细胞的增殖，进一步促进了胶质瘤的发生和发展。因此，CEP55可能是治疗胶质瘤的一个新的治疗靶点。
