Source:http://linkedlifedata.com/resource/pubmed/id/17671689
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-8-2
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pubmed:abstractText |
Type I interferon (IFN) was originally identified as an immunomodulatory cytokine because of its antiviral activity. Further characterization of its biological effects revealed a prominent role in the direct control of cell growth and potent immunomodulatory and antiangiogenic actions. IFN-alpha and IFN-beta had both been classified as type I IFN, but differences in their antitumor activities were reported. We confirmed the difference in the antiproliferative activities of IFN-alpha2b and IFN-beta toward HT29 and SW480 cells. IFN treatment was observed to prolong cell cycle progression; in particular, the accumulation of S-phase population was one of the most characteristic changes. The prolongation of S-phase progression and transition into G2/M-phase was suggested to be a crucial action of type I IFN on colon cancer. Additionally, IFN activated the p21 promoter gene and induced p21WAF1/CIP1 expression. Furthermore, the cell cycle prolongation effect of IFN was suppressed when p21 expression was downregulated. Therefore, we confirmed that p21WAF1/CIP1 was a crucial target molecule for the effects of IFN on the cell cycle. Additionally, the ability of p21 induction differed between IFN-alpha2b and IFN-beta and correlated with their inhibitory activities toward cell growth. We conclude that type I IFN prolongs cell cycle progression by p21WAF1/CIP1 induction in human colon cancer cells.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/interferon alfa-2b
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1019-6439
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
613-20
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:17671689-Apoptosis,
pubmed-meshheading:17671689-Cell Cycle,
pubmed-meshheading:17671689-Cell Line, Tumor,
pubmed-meshheading:17671689-Cell Proliferation,
pubmed-meshheading:17671689-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:17671689-Disease Progression,
pubmed-meshheading:17671689-Enzyme Inhibitors,
pubmed-meshheading:17671689-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17671689-Humans,
pubmed-meshheading:17671689-Interferon Type I,
pubmed-meshheading:17671689-Interferon-alpha,
pubmed-meshheading:17671689-Interferon-beta,
pubmed-meshheading:17671689-RNA Interference,
pubmed-meshheading:17671689-Recombinant Proteins,
pubmed-meshheading:17671689-S Phase
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pubmed:year |
2007
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pubmed:articleTitle |
Type I interferon prolongs cell cycle progression via p21WAF1/CIP1 induction in human colon cancer cells.
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pubmed:affiliation |
Department of General Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan. tomonari@f4.dion.ne.jp
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pubmed:publicationType |
Journal Article
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