Source:http://linkedlifedata.com/resource/pubmed/id/19885619
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2009-11-3
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pubmed:abstractText |
The reduced expression in immortalized cells (REIC)/Dickkopf (Dkk)-3, a member of the Dkk gene family, is a tumor suppressor in a broad range of cancers. REIC/Dkk-3 transfected stable clones of mouse prostate cancer RM9 cells (RM9-REIC) and the empty vector-transfected control clone cells (RM9-EV) were established. Clones were used to evaluate the anti-cancer effects and a proteomics analysis of REIC/Dkk-3 continuous expression was performed. The RM9-REIC cells show a feeble appearance and the cell membrane shows irregular buds known as blebs. In vitro cell proliferation was significantly suppressed in RM9-REIC clones in comparison to the control. The apoptosis assay was done under standard culture conditions and RM9-REIC showed a higher incidence of apoptosis. The RM9-EV and RM9-REIC cells were orthotopically implanted into a C57BL/6 mouse prostate. After 2 weeks, the tumor growth was significantly inhibited in RM9-REIC cells in comparison to the control. Two-dimensional gel electrophoresis was used to examine the modification of protein expression by the gene transfection. The analysis with mass spectrometry disclosed that expression of peroxiredoxin-1, GST-P1, transgelin-2, MRP-L12, ARD, GRP78 and Sorcin were increased and eEF1A-1 and cyclophilin-40 protein were decreased in RM9-REIC cells. Therefore, REIC/Dkk-3 stable transfectants show a reduction of malignancy in mouse prostate cancer RM9 cells in vitro and in vivo. The result of the proteomics analysis might provide important clues to clarify the anti-cancer molecular mechanism of REIC/Dkk-3 gene transfer.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1791-244X
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pubmed:author |
pubmed-author:ChenJieJ,
pubmed-author:HuangPengP,
pubmed-author:HuhNam-HoNH,
pubmed-author:KakuHarukiH,
pubmed-author:KashiwakuraYujiY,
pubmed-author:KumonHiromiH,
pubmed-author:NasuYasutomoY,
pubmed-author:OchiaiKazuhikoK,
pubmed-author:OuchidaMamoruM,
pubmed-author:SakaguchiMasakiyoM,
pubmed-author:ShimizuKenjiK,
pubmed-author:WatanabeMasamiM
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pubmed:issnType |
Electronic
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
789-94
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pubmed:meshHeading |
pubmed-meshheading:19885619-Animals,
pubmed-meshheading:19885619-Apoptosis,
pubmed-meshheading:19885619-Blotting, Western,
pubmed-meshheading:19885619-Cell Growth Processes,
pubmed-meshheading:19885619-Cell Line, Tumor,
pubmed-meshheading:19885619-Cell Membrane,
pubmed-meshheading:19885619-Cell Survival,
pubmed-meshheading:19885619-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:19885619-Male,
pubmed-meshheading:19885619-Mice,
pubmed-meshheading:19885619-Mice, Inbred C57BL,
pubmed-meshheading:19885619-Neoplasm Transplantation,
pubmed-meshheading:19885619-Phenotype,
pubmed-meshheading:19885619-Prostatic Neoplasms,
pubmed-meshheading:19885619-Proteomics,
pubmed-meshheading:19885619-Transfection,
pubmed-meshheading:19885619-Tumor Burden
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pubmed:year |
2009
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pubmed:articleTitle |
REIC/Dkk-3 stable transfection reduces the malignant phenotype of mouse prostate cancer RM9 cells.
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pubmed:affiliation |
Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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