Source:http://linkedlifedata.com/resource/pubmed/id/19879751
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2009-12-16
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pubmed:abstractText |
Signal pathways of novel type III interferons (IFN-lambdas) are similar to those of type I IFNs (IFN-alpha/beta) but their distinct functions have not been well characterised. We examined the growth suppressive activity of IFN-lambda1 with nine human oesophageal carcinoma cell lines expressing the IFN-lambda receptor complexes. Among them, three lines but not others showed IFN-lambda1-mediated growth suppression by inducing G1 phase arrest or apoptosis. The G1 phase arrest was accompanied by the up-regulation of p21 and dephosphorylation of retinoblastoma (Rb), and the apoptosis was evidenced by cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP). Similar but not identical susceptibility was found in IFN-alpha-treated oesophageal carcinoma cells. Despite the differential suppressive responses among the cells, all the cells increased the expression of the myxovirus resistance A (MxA) and 2',5'-oligoadenylate synthetase (2',5'-OAS) genes and class I antigens of the major histocompatibility complexes (MHC) with IFN-lambda1 treatment. Fibroblasts and mesenchymal stem cells, positive for IFN-alpha receptor (IFNAR), lacked one of the IFN-lambda receptor complexes and Het-1A, immortalised oesophageal epithelium cells, were insensible to the IFN-lambda1-induced growth suppression. IFN-lambda1 produced combinatory anti-tumour effects with chemotherapeutic agents, cisplatin (CDDP) and 5-fluorouracil (5-FU), in IFN-lambda1-sensitive oesophageal carcinoma cells but not in normal or Het-1A cells, while IFN-alpha achieved the combinatory suppressive effects to normal cells. These data collectively show that IFN-lambda1 responsiveness is tissue-specific due to the restricted receptors expression and is diversified even among cells of the same lineage, and suggest that IFN-lambda1 is a potential therapeutic agent for oesophageal carcinoma without damaging surrounding tissues.
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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/IL10RB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IL29 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10 Receptor beta Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytokine,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin 28alpha receptor
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1879-0852
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
46
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
180-90
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pubmed:meshHeading |
pubmed-meshheading:19879751-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:19879751-Apoptosis,
pubmed-meshheading:19879751-Cell Cycle,
pubmed-meshheading:19879751-Cell Proliferation,
pubmed-meshheading:19879751-Drug Evaluation, Preclinical,
pubmed-meshheading:19879751-Esophageal Neoplasms,
pubmed-meshheading:19879751-G1 Phase,
pubmed-meshheading:19879751-Humans,
pubmed-meshheading:19879751-Interleukin-10 Receptor beta Subunit,
pubmed-meshheading:19879751-Interleukins,
pubmed-meshheading:19879751-Receptors, Cytokine,
pubmed-meshheading:19879751-Recombinant Proteins,
pubmed-meshheading:19879751-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19879751-Tumor Cells, Cultured
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pubmed:year |
2010
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pubmed:articleTitle |
Interferon-lambda induces G1 phase arrest or apoptosis in oesophageal carcinoma cells and produces anti-tumour effects in combination with anti-cancer agents.
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pubmed:affiliation |
Division of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, Chiba 260-8717, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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