NDLI: CEP55 contributes to human gastric carcinoma by regulating cell proliferation

Content Provider	Springer Nature Link
Author	Tao, Jinqiu Zhi, Xiaofei Tian, Yuan Li, Zheng Zhu, Yi Wang, Weizhi Xie, Kunling Tang, Jie Zhang, Xiaoyu Wang, Linjun Xu, Zekuan
Copyright Year	2014
Abstract	Centrosomal protein 55 (CEP55) is the latest found member in the centrosomal relative protein family, which participates in cell-cycle regulation. CEP55 exists in many kinds of normal tissues and tumour cells such as hepatocellular carcinoma, and is important in carcinogenesis. However, the role of CEP55 in the pathogenesis of gastric cancer (GC) remains unclear. The mRNA levels of CEP55 in GC tissues and GC cell lines were examined by quantitative real-time PCR, and the protein expression of CEP55 in GC tissues was detected by Western blot and immunohistochemistry. The role of CEP55 in regulating the proliferation of GC cell lines was investigated both in vitro and in vivo. CEP55 was strongly upregulated in human GC, indicating that CEP55 contributed to carcinogenesis and progression of GC. Ectopic overexpression of CEP55 enhanced the cell proliferation, colony formation, and tumourigenicity of GC cells, whereas CEP55 knockdown inhibited these effects. We discovered that cell transformation induced by CEP55 was mediated by the AKT signalling pathway. Overexpression of CEP55 enhanced the phosphorylation of AKT and inhibited the activity of p21 WAF1/Cip1. In addition, cellular proliferation was suppressed as a result of cell cycle arrest at the G2/M phase in CEP55-knockdown cells. CEP55 expression was elevated in GC compared with normal control tissues. Credible evidence showed that CEP55 can be a potential therapeutic target in GC.
Starting Page	4389
Ending Page	4399
Page Count	11
File Format	PDF
ISSN	10104283
Journal	Tumor Biology
Volume Number	35
Issue Number	5
e-ISSN	14230380
Language	English
Publisher	Springer Netherlands
Publisher Date	2014-01-04
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Gastric cancer CEP55 Proliferation PI3K/AKT/p21 Cell cycle Cancer Research
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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