Source:http://linkedlifedata.com/resource/pubmed/id/19891584
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2009-11-6
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pubmed:abstractText |
OBJECTIVE. miR-122 is highly abundant in liver and a hepato-specific microRNA. There is evidence to show that miR-122 expression is down-regulated in human hepatocellular carcinoma (HCC). It is not known whether miR-122 affects the cellular behavior of hepatoma cells. The aim of this study was to investigate the effects of miR-122 on the viability and apoptosis of hepatoma cells. MATERIAL AND METHODS. The viability and apoptosis of Huh-7 and HepG2 cells treated with miR-122 or miR-122 antisense RNA (anti-miR-122) were analyzed by adenosine triphosphate (ATP)-based luminescent assay, annexin V-based flow cytometry, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) detection. The miR-122 coding genes in both cell lines were sequenced. RESULTS. Although two putative promoter sequences for the miR-122 gene at 18q21.31 were detected, the miR-122 coding sequence was missing in HepG2 cells, which might be the reason for the absence of miR-122 expression. There was no significant difference between the viabilities of HepG2 cells transfected with miR-122 and mock HepG2 cells (p >0.05). However, the viability of Huh-7 transfected with anti-miR-122 was significantly elevated at 24, 36, and 48 h posttransfection compared with that of mock cells (p <0.01). Both the flow cytometry and TUNEL assay showed that the apoptotic level of Huh-7 transfected with anti-miR-122 was significantly decreased at 48 h posttransfection (p <0.01). CONCLUSIONS. miR-122 down-regulated the viability but up-regulated the apoptosis of hepatoma cell Huh-7. The absence of miR-122 expression in HepG2 cells was due to the loss of the miR-122 coding sequence in chromosome 18. These results imply that aberrant expression of miR-122 may contribute to hepatocarcinogenesis.
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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:issn |
1502-7708
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1332-9
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pubmed:meshHeading |
pubmed-meshheading:19891584-Apoptosis,
pubmed-meshheading:19891584-Carcinoma, Hepatocellular,
pubmed-meshheading:19891584-Cell Line, Tumor,
pubmed-meshheading:19891584-Cell Survival,
pubmed-meshheading:19891584-Flow Cytometry,
pubmed-meshheading:19891584-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:19891584-Humans,
pubmed-meshheading:19891584-In Situ Nick-End Labeling,
pubmed-meshheading:19891584-Liver Neoplasms,
pubmed-meshheading:19891584-MicroRNAs,
pubmed-meshheading:19891584-RNA, Neoplasm,
pubmed-meshheading:19891584-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
2009
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pubmed:articleTitle |
miR-122 affects the viability and apoptosis of hepatocellular carcinoma cells.
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pubmed:affiliation |
Department of Microbiology, Harbin Medical University, Harbin, Heilongjiang, China.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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