Document Detail


Identification of metastasis-associated proteins involved in gallbladder carcinoma metastasis by proteomic analysis and functional exploration of chloride intracellular channel 1.
MedLine Citation:
PMID:  19299076     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Advanced gallbladder cancer has an extremely poor prognosis because of metastasis. Identification of metastasis-related biomarkers is essential to improve patient survival. In the present study, metastasis-associated proteins were identified by comparative proteomic analysis and the metastasis-related function of the candidate protein, chloride intracellular channel 1 (CLIC1), was further elucidated. Two cell lines with high or low metastatic potential (termed GBC-SD18H and GBC-SD18L, respectively), originating from the same parental gallbladder carcinoma GBC-SD cell line, were identified by spontaneous metastasis in vivo and characterized by metastatic phenotypes analysis in vitro. Subsequently, a proteomic approach comprised of two-dimensional gel electrophoresis analysis and mass spectroscopy was used to identify and compare the protein expression patterns between GBC-SD18L and GBC-SD18H. Twenty-six proteins were identified and further verified by one-dimensional Western blotting and semiquantitative reverse transcriptase polymerase chain reaction analysis. It was determined that CLIC1, ezrin, vimentin, annexin A3, WD repeat domain 1, triosephosphate isomerase, C1-tetrahydrofolate synthase, Rho GDP-dissociation inhibitor 1, T-complex protein 1, heterogeneous nuclear ribonucleoprotein K, glutamate dehydrogenase 1, proteasome activator complex subunit 3 and Rab GDP-dissociation inhibitor beta were significantly up-regulated in the highly metastatic GBC-SD18H cell line compared to the poorly metastatic GBC-SD18L cell line. However, phosphoglycerate kinase 1 and programmed cell death protein 8 were significantly down-regulated in the highly metastatic GBC-SD18H cell line compared to GBC-SD18L. Considering that CLIC1 was profuse in highly metastatic GBC-SD18H but scarce in poorly metastatic GBC-SD18L, the association of CLIC1 with metastasis was further elucidated by the overexpression and RNA interference of CLIC1 in GBC-SD18L cells and GBC-SD18H cells, respectively. The results demonstrated that the overexpression of CLIC1 promoted cell motility and invasion of GBC-SD18L in vitro, while RNA interference of CLIC1 remarkably decreased cell motility and invasive potency of GBC-SD18H in vitro, indicating that CLIC1 might play an important role in metastasis of gallbladder carcinoma.
Authors:
Jian-Wei Wang; Shu-You Peng; Jiang-Tao Li; Yong Wang; Zhi-Ping Zhang; Yan Cheng; De-Qing Cheng; Wei-Hong Weng; Xiang-Song Wu; Xiao-Zhou Fei; Zhi-Wei Quan; Ji-Yu Li; Song-Gang Li; Ying-Bin Liu
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-18
Journal Detail:
Title:  Cancer letters     Volume:  281     ISSN:  1872-7980     ISO Abbreviation:  Cancer Lett.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-06-08     Completed Date:  2009-06-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7600053     Medline TA:  Cancer Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  71-81     Citation Subset:  IM    
Affiliation:
Department of Surgery, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carcinoma / pathology,  secondary*
Cell Line, Tumor
Cell Movement / drug effects
Chloride Channels / antagonists & inhibitors,  genetics,  physiology*
Gallbladder Neoplasms / pathology*
Gene Expression Profiling
Humans
Liver Neoplasms / secondary
Male
Mice
Mice, Inbred BALB C
Mice, Nude
Neoplasm Invasiveness / physiopathology*
Neoplasm Proteins / antagonists & inhibitors,  biosynthesis,  genetics,  physiology*
Neoplasm Transplantation
Proteomics
RNA Interference
Recombinant Fusion Proteins / physiology
Specific Pathogen-Free Organisms
Chemical
Reg. No./Substance:
0/CLIC1 protein, human; 0/Chloride Channels; 0/Neoplasm Proteins; 0/Recombinant Fusion Proteins

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