| Identification of metastasis-associated proteins involved in gallbladder carcinoma metastasis by proteomic analysis and functional exploration of chloride intracellular channel 1. | |
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MedLine Citation:
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PMID: 19299076 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2009-03-18 |
Journal Detail:
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Title: Cancer letters Volume: 281 ISSN: 1872-7980 ISO Abbreviation: Cancer Lett. Publication Date: 2009 Aug |
Date Detail:
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Created Date: 2009-06-08 Completed Date: 2009-06-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7600053 Medline TA: Cancer Lett Country: Ireland |
Other Details:
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Languages: eng Pagination: 71-81 Citation Subset: IM |
Affiliation:
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Department of Surgery, Second Affiliated Hospital, Zhejiang University, Hangzhou, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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0/CLIC1 protein, human; 0/Chloride Channels; 0/Neoplasm Proteins; 0/Recombinant Fusion Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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