Document Detail


Molecular mechanism of chemoresistance by astrocyte elevated gene-1.
MedLine Citation:
PMID:  20388796     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our recent findings show that astrocyte elevated gene-1 (AEG-1) is overexpressed in >90% of human hepatocellular carcinoma (HCC) samples, and AEG-1 plays a central role in regulating development and progression of HCC. In the present study, we elucidate a molecular mechanism of AEG-1-induced chemoresistance, an important characteristic of aggressive cancers. AEG-1 increases the expression of multidrug resistance gene 1 (MDR1) protein, resulting in increased efflux and decreased accumulation of doxorubicin, promoting doxorubicin resistance. Suppression of MDR1 by small interfering RNA or chemical reagents, or inhibition of AEG-1 or a combination of both genes, significantly increases in vitro sensitivity to doxorubicin. In nude mice xenograft studies, a lentivirus expressing AEG-1 short hairpin RNA, in combination with doxorubicin, profoundly inhibited growth of aggressive human HCC cells compared with either agent alone. We document that although AEG-1 does not affect MDR1 gene transcription, it facilitates association of MDR1 mRNA to polysomes, resulting in increased translation, and AEG-1 also inhibits ubiquitination and subsequent proteasome-mediated degradation of MDR1 protein. This study is the first documentation of a unique aspect of AEG-1 function (i.e., translational and posttranslational regulation of proteins). Inhibition of AEG-1 might provide a means of more effectively using chemotherapy to treat HCC, which displays inherent chemoresistance with aggressive pathology.
Authors:
Byoung Kwon Yoo; Dong Chen; Zhao-Zhong Su; Rachel Gredler; Jinsang Yoo; Khalid Shah; Paul B Fisher; Devanand Sarkar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-04-13
Journal Detail:
Title:  Cancer research     Volume:  70     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-16     Completed Date:  2010-04-28     Revised Date:  2012-04-04    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3249-58     Citation Subset:  IM    
Copyright Information:
(c) 2010 AACR.
Affiliation:
Department of Human and Molecular Genetics, VCU Institute of Molecular Medicine, and VCU Massey Cancer Center, Virginia Commonwealth University, School of Medicine, Richmond, Virginia 23298, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carcinoma, Hepatocellular / enzymology*
Cell Adhesion Molecules / biosynthesis*,  physiology*
Cell Line, Tumor
Doxorubicin / pharmacology
Gene Expression Regulation, Neoplastic*
Humans
Lentivirus / genetics
Liver Neoplasms / enzymology*
Mice
Mice, Nude
Neoplasm Transplantation
P-Glycoprotein / metabolism
RNA, Messenger / metabolism
RNA, Small Interfering / metabolism
Grant Support
ID/Acronym/Agency:
R01 CA035675/CA/NCI NIH HHS; R01 CA035675-22/CA/NCI NIH HHS; R01 CA134721/CA/NCI NIH HHS; R01 CA134721-01A1/CA/NCI NIH HHS; R01 CA134721-04/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/ABCB1 protein, human; 0/Cell Adhesion Molecules; 0/MTDH protein, human; 0/P-Glycoprotein; 0/RNA, Messenger; 0/RNA, Small Interfering; 23214-92-8/Doxorubicin
Comments/Corrections

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