Document Detail


Antitumor progression potential of caffeic acid phenethyl ester involving p75(NTR) in C6 glioma cells.
MedLine Citation:
PMID:  20836997     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The previous data showed that caffeic acid phenethyl ester (CAPE), a component of propolis, possesses inducing cell cycle arrest and antiproliferation effect on C6 glioma cells in vitro and in vivo. In the present study, C6 glioma cells treated with CAPE resulted in morphological changes to an astrocytic phenotype and increased the expression of glial differentiation marker proteins including glial fibrillary acidic protein (GFAP) and S-100β. In addition, with scratch assay and Boyden chamber assay, CAPE exhibited inhibitory effects on the motility and invasion of C6 glioma cells. Furthermore, CAPE induced the expression of nerve growth factor (NGF) and p75 neurotrophin receptor (p75(NTR)), which were involved in neural cell differentiation. CAPE could also inhibit the activity of matrix metalloproteinases (MMPs) and induce the expression of RhoB, a tumor suppressor. To examine the involvement of p75(NTR) in the anti-invasive property of CAPE, Western blotting and Boyden Chamber assay were performed by addition of an anti-p75(NTR) antibody in C6 cells. The results showed that blocking p75(NTR) could decrease the CAPE-induced expression of RhoB and the inactivation of MMP-2, -9 as well as the anti-invasion effect in C6 glioma cells. Furthermore, CAPE suppressed IκB-α phosphorylation which was down stream of p75(NTR). Finally, the effect of CAPE on metastasis by lung colonization of the tumor cell in nude mice was also evaluated. It was found that the groups of nude mice injected with CAPE-pretreated cells could decrease both lung size and weight as compared to the positive control group which did not receive CAPE treatment. In addition, histological examination of the mouse lung sections showed that the CAPE-treated group inhibited the metastasis of C6 glioma cells. These data suggest CAPE possesses antitumor progression potential.
Authors:
Wea-Lung Lin; Wen-Hai Liang; Yean-Jang Lee; Shien-Kai Chuang; Tsui-Hwa Tseng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-15
Journal Detail:
Title:  Chemico-biological interactions     Volume:  188     ISSN:  1872-7786     ISO Abbreviation:  Chem. Biol. Interact.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-12     Completed Date:  2010-12-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0227276     Medline TA:  Chem Biol Interact     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  607-15     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Department of Pathology, Chung Shan Medical University Hospital, Taichung, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / immunology
Antineoplastic Agents / pharmacology*
Biological Markers / metabolism
Caffeic Acids / pharmacology*
Cell Differentiation / drug effects
Cell Line, Tumor
Cell Movement / drug effects
Cell Proliferation / drug effects
Disease Progression*
Down-Regulation / drug effects
Gene Expression Regulation, Neoplastic / drug effects
Glioma / genetics,  metabolism,  pathology*
I-kappa B Kinase / metabolism
Lung / drug effects,  pathology
Matrix Metalloproteinases / metabolism
Mice
Mice, Nude
Neoplasm Invasiveness
Neoplasm Metastasis
Nerve Growth Factor / metabolism
Neuroglia / drug effects,  metabolism,  pathology
Phenylethyl Alcohol / analogs & derivatives*,  pharmacology
Phosphorylation / drug effects
Rats
Receptor, Nerve Growth Factor / immunology,  metabolism*
rhoB GTP-Binding Protein / metabolism
Chemical
Reg. No./Substance:
0/Antibodies; 0/Antineoplastic Agents; 0/Biological Markers; 0/Caffeic Acids; 0/Receptor, Nerve Growth Factor; 104594-70-9/caffeic acid phenethyl ester; 60-12-8/Phenylethyl Alcohol; 9061-61-4/Nerve Growth Factor; EC 2.7.11.10/I-kappa B Kinase; EC 3.4.24.-/Matrix Metalloproteinases; EC 3.6.5.2/rhoB GTP-Binding Protein

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