title: CEP55 contributes to human gastric carcinoma by regulating cell proliferation.
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.
authors.affiliation: Division of Gastric Surgery, Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
authors.forename: Jinqiu
authors.initials: J
authors.lastname: Tao
authors.forename: Xiaofei
authors.initials: X
authors.lastname: Zhi
authors.forename: Yuan
authors.initials: Y
authors.lastname: Tian
authors.forename: Zheng
authors.initials: Z
authors.lastname: Li
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Weizhi
authors.initials: W
authors.lastname: Wang
authors.forename: Kunling
authors.initials: K
authors.lastname: Xie
authors.forename: Jie
authors.initials: J
authors.lastname: Tang
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Zhang
authors.forename: Linjun
authors.initials: L
authors.lastname: Wang
authors.forename: Zekuan
authors.initials: Z
authors.lastname: Xu
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D059447:Cell Cycle Checkpoints; D018797:Cell Cycle Proteins / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D008875:Middle Aged; D009687:Nuclear Proteins / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology; D015398:Signal Transduction; D013274:Stomach Neoplasms / Q000209:etiology / Q000473:pathology*
chemical_list: C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; C505378:Cep55 protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D009687:Nuclear Proteins; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt