title: Overexpression of candidate tumor suppressor ECRG4 inhibits glioma proliferation and invasion.
abstract: BACKGROUND
  ECRG4 has been shown to be a candidate tumor suppressor in several tumors, but its role in glioma remains poorly understood. In this study, we examined the mRNA expression of ECRG4 and investigated its biological role in glioma cells.
  
  
  METHODS
  Real-time PCR was used to examine expression of ECRG4 in gliomas and their matched brain tissues. The effect of ECRG4 expression on cell proliferation, invasion, and migration was investigated in human U251 glioma cells. Finally, the regulation of transcription factor NF-kB by ECRG4 was evaluated by western blotting.
  
  
  RESULTS
  Of the 10 paired samples analyzed, 9 glioma tissues displayed the decreased expression of ECRG4 compared to matched normal brain tissues. Cells transfected with ECRG4 showed significantly decreased cell proliferation as evaluated by MTT and colony formation assays. Furthermore, overexpression inhibited cell migration and invasion in transwell and Boyden chamber experiments and retarded the cell cycle progression from G1 to S phase by FACSCaliber cytometry. Protein levels of nuclear transcription factor NF-kB, which is involved in cell proliferation, inversely correlated with ECRG4 expression.
  
  
  CONCLUSIONS
  Our data suggest that ECRG4 serves as a tumor suppressor in glioma.
authors.affiliation: The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 130021, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Xinrui
authors.initials: X
authors.lastname: Liu
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Dongxue
authors.initials: D
authors.lastname: Qi
authors.forename: Lihong
authors.initials: L
authors.lastname: Zhang
authors.forename: Yuhong
authors.initials: Y
authors.lastname: Jin
authors.forename: Hongfa
authors.initials: H
authors.lastname: Yang
mesh_terms: D015153:Blotting, Western; D001932:Brain Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control*; D016022:Case-Control Studies; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control*; D006801:Humans; D007124:Immunoenzyme Techniques; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D011379:Prognosis; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014407:Tumor Cells, Cultured; D025521:Tumor Suppressor Proteins
chemical_list: C476999:ECRG4 protein, human; D016328:NF-kappa B; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D025521:Tumor Suppressor Proteins