title: Suppression of C6 gliomas via application of rat hyperplasia gene.
abstract: BACKGROUND
  Among all neurological tumors, tumor incidence of the neuroepithelial tissue is the highest, where 50% are gliomas. Treatment for gliomas has traditionally included surgery and adjuvant therapy. With advancements in medicine, gene therapy has entered the clinical setting, in which control of tumor growth, tumor volume and decrease of supply of blood to the tumor have been observed. Rat hyperplasia suppressor gene (rHSG) has been proven to inhibit the injury-mediated proliferation of vascular smooth muscle cells.
  
  
  METHODS
  A recombinant adenovirus, Adv-rHSG-GFP, was constructed and characterized by in vitro and in vivo studies. The function of rHSG on cell proliferation was determined in vitro by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) exclusion assay and plate clone formation, while a C6/Sprague Dawley rat glioma model was established to observe the effect of rHSG in vivo.
  
  
  RESULTS
  Overexpression of rHSG displayed a strong effect on suppressing C6 cells proliferation in vitro and growth of glioma in vivo, which suggests the use of rHSG as a possible treatment strategy for glioma. p21Cip1, p27Kip1 and proliferating cell nuclear antigen were found to be involved in the tumor suppression mechanism of rHSG.
  
  
  CONCLUSIONS
  rHSG can markedly inhibit of the growth of rat glioma cells. The suppression mechanism of rHSG may be related to cell cycle regulation, which shows that rHSG is a potential therapeutic target of glioma tumor. This preclinical study supports a further in-depth study on the effect of rHSG on cell proliferation, migration and change in the extracellular matrix component of glioma cells.
authors.affiliation: 2 Ningxia Medical University, Ningxia - PR China.
authors.forename: Peng
authors.initials: P
authors.lastname: Gao
authors.forename: Zhanwei
authors.initials: Z
authors.lastname: Wang
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.forename: Yourui
authors.initials: Y
authors.lastname: Zou
authors.forename: Hui
authors.initials: H
authors.lastname: Guo
authors.forename: Haibo
authors.initials: H
authors.lastname: Liu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Yang
authors.forename: Zhihao
authors.initials: Z
authors.lastname: Fang
authors.forename: Shucai
authors.initials: S
authors.lastname: Jiang
authors.forename: Bing
authors.initials: B
authors.lastname: Shen
authors.forename: Louis W C
authors.initials: LW
authors.lastname: Chow
authors.forename: Wings Tjing-yung
authors.initials: WT
authors.lastname: Loo
authors.forename: Elizabeth L Y
authors.initials: EL
authors.lastname: Ng
authors.forename: William W N
authors.initials: WW
authors.lastname: Tsang
mesh_terms: D000256:Adenoviridae / Q000235:genetics; D000818:Animals; D059447:Cell Cycle Checkpoints / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000235:genetics; D020558:GTP Phosphohydrolases; D015316:Genetic Therapy / Q000379:methods*; D005910:Glioma / Q000235:genetics* / Q000628:therapy*; D057809:HEK293 Cells; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D024101:Mitochondrial Proteins / Q000235:genetics*; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C493958:Cdkn1a protein, rat; D050759:Cyclin-Dependent Kinase Inhibitor p21; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D018809:Proliferating Cell Nuclear Antigen; D050760:Cyclin-Dependent Kinase Inhibitor p27; D020558:GTP Phosphohydrolases; C489710:Mfn2 protein, rat