title: Phosphatase of regenerating liver-3 induces angiogenesis by increasing extracellular signal-regulated kinase phosphorylation in endometrial adenocarcinoma.
abstract: OBJECTIVE
  The aim of this study was to investigate the mechanism by which phosphatase of regenerating liver-3 (PRL-3) induces angiogenesis in endometrial adenocarcinoma tissues and cells.
  
  
  METHODS
  We investigated the expression of PRL-3 and vascular endothelial growth factor (VEGF) in samples from 124 patients with endometrial adenocarcinoma using immunohistochemical staining. The relationship between PRL-3 expression and microvessel density (MVD), clinicopathological factors and surgical treatment outcome was also studied. Following this, we studied the effect on cell lines of blocking or upregulating PRL-3.
  
  
  RESULTS
  PRL-3 expression in endometrial adenocarcinoma was high, and this overexpression is correlated with advanced clinical stage (p=0.008), lymph node metastasis (p=0.016) and poor postoperative survival. PRL-3 overexpression was associated with VEGF (p=0.001) expression and MVD (p=0.005). Upregulating PRL-3 expression promoted VEGF and phosphorylated extracellular signal-regulated kinase (pERK) expression. Blocking PRL-3 expression inhibited VEGF and pERK expression. Following inhibition of pERK, VEGF expression was downregulated.
  
  
  CONCLUSIONS
  PRL-3 induces microvascular vessel formation by facilitating VEGF expression in endometrial adenocarcinoma tissues. PRL-3 upregulates pERK expression and activity, facilitating VEGF expression and accelerating angiogenesis.
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, Shenyang, PR China.
authors.forename: Jian
authors.initials: J
authors.lastname: Ming
authors.forename: Yanduo
authors.initials: Y
authors.lastname: Jiang
authors.forename: Guocheng
authors.initials: G
authors.lastname: Jiang
authors.forename: Huachuan
authors.initials: H
authors.lastname: Zheng
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology* / Q000401:mortality / Q000473:pathology; D014408:Biomarkers, Tumor / Q000032:analysis; D015153:Blotting, Western; D016889:Endometrial Neoplasms / Q000201:enzymology* / Q000401:mortality / Q000473:pathology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D053208:Kaplan-Meier Estimate; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000201:enzymology*; D010766:Phosphorylation; D011379:Prognosis; D017027:Protein Tyrosine Phosphatases / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
chemical_list: D014408:Biomarkers, Tumor; D009363:Neoplasm Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D048049:Extracellular Signal-Regulated MAP Kinases; C484730:PTP4A3 protein, human; D017027:Protein Tyrosine Phosphatases