Document Detail


Axin induces cell death and reduces cell proliferation in astrocytoma by activating the p53 pathway.
MedLine Citation:
PMID:  19513548     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Astrocytic tumors are the most common brain tumors with various genetic defects. As a tumor suppressor gene, Axin could control cell death and growth. Axin possesses a separate domain that directly interacts with p53 and regulates the activity of p53 pathway. Our aims were to elucidate the effects of Axin on the progression of astrocytoma. We examined the expression of Axin in 96 cases of astrocytoma using immunohistochemistry. The apoptotic index, proliferactive acitivity and the expression levels of p53 and its downstream genes, p21 and Cyclin D1, were evaluated in the C6 astrocytoma cells with overexpression or silencing of Axin. The results showed the levels of Axin correlated significantly inversely with the grades of astrocytoma (R=-0.286, P<0.05) and correlated negatively with Ki-67 labeling index (R=-0.227, P<0.05). Overexpression of Axin in C6 cells induces cell death, and reduces the cell proliferation, up-regulates the expression of p53. Silencing of Axin reduces p53 expression. The p53 inhibitor, pifithrin-alpha, was able to counteract the effect of Axin in C6 cells. Our data demonstrate that the expression of Axin is associated negatively with the progression of astrocytoma. In conclusion, Axin induces cell death and reduces cell proliferation, partially by activating the p53 pathway in astrocytoma cells. This knowledge is helpful in understanding the role of Axin in the progression of astrocytoma.
Authors:
Li-Ying Zhang; Jing Ye; Feng Zhang; Fan-Fan Li; Hang Li; Yu Gu; Fang Liu; Guang-Sheng Chen; Qing Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of oncology     Volume:  35     ISSN:  1019-6439     ISO Abbreviation:  Int. J. Oncol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-10     Completed Date:  2009-08-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9306042     Medline TA:  Int J Oncol     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  25-32     Citation Subset:  IM    
Affiliation:
State Key Laboratory of Cancer Biology and Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, P.R. China.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Animals
Apoptosis* / drug effects
Astrocytoma / genetics,  metabolism*,  pathology
Benzothiazoles / pharmacology
Brain Neoplasms / genetics,  metabolism*,  pathology
Cell Line, Tumor
Cell Proliferation* / drug effects
Child
Child, Preschool
Cyclin D1 / metabolism
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Female
Glioblastoma / metabolism*,  pathology
Humans
Immunohistochemistry
Male
Middle Aged
Neoplasm Staging
RNA Interference
Rats
Repressor Proteins / genetics,  metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Time Factors
Toluene / analogs & derivatives,  pharmacology
Transfection
Tumor Suppressor Protein p53 / antagonists & inhibitors,  metabolism*
Young Adult
Chemical
Reg. No./Substance:
0/Axin protein; 0/Benzothiazoles; 0/Ccnd1 protein, rat; 0/Cdkn1a protein, rat; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Repressor Proteins; 0/Tumor Suppressor Protein p53; 0/pifithrin; 108-88-3/Toluene; 136601-57-5/Cyclin D1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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