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Title: Suppression of C6 gliomas via application of rat hyperplasia gene
Authors: Gao, P
Wang, Z
Zhang, B
Zou, Y
Guo, H
Liu, H
Yang, Q
Fang, Z
Jiang, S
Shen, B
Chow, LWC
Loo, WTY
Tsang, WWN 
Keywords: Adenovirus
Rat hyperplasia suppressor gene
Issue Date: 2014
Publisher: Wichtig Editore
Source: International journal of biological markers, 2014, v. 29, no. 4, p. e411-e422 How to cite?
Journal: International journal of biological markers 
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.
ISSN: 0393-6155
DOI: 10.5301/jbm.5000114
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