Source:http://linkedlifedata.com/resource/pubmed/id/17513614
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2007-5-21
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pubmed:abstractText |
Deregulated signaling by the epidermal growth factor receptor family of proteins is encountered in human malignancies including breast cancer. Cell cycle and apoptosis-regulatory protein-1 (CARP-1), a novel, perinuclear phosphoprotein, is a regulator of apoptosis signaling by epidermal growth factor receptors. CARP-1 expression is diminished in human breast cancers, and correlates inversely with human breast cancer grades which could be attributed to increased methylation. The expression of CARP-1, on the other hand, interferes with the ability of human breast cancer cells to invade through the matrigel-coated membranes, to form colonies in the soft agar, and to grow as s.c. tumors in severe combined immunodeficiency (SCID) mice. To test whether CARP-1 is a suppressor of human breast cancer growth, we generated transactivator of transcription (TAT)-tagged CARP-1 peptides. Treatment of human breast cancer cells with affinity purified, TAT-CARP-1 1-198, 197-454, and 896-1150 peptides caused inhibition of human breast cancer cell proliferation and elevated apoptosis. In contrast, TAT-tagged enhanced green fluorescent protein or CARP-1 (1-198(Y192/F)) peptide failed to inhibit cell proliferation or induce apoptosis. Apoptosis by CARP-1 peptides, with the exception of CARP-1 (1-198(Y192/F)), involves the activation of p38 stress-activated protein kinase and caspase-9. Moreover, administration of TAT-CARP-1 (1-198), but not TAT-tagged enhanced green fluorescent protein or TAT-CARP-1 (1-198(Y192/F)), inhibits growth of human breast cancer cell-derived tumor xenografts in SCID mice. We conclude that CARP-1 is a suppressor of human breast cancer growth, and its expression is diminished in tumors, in part, by methylation-dependent silencing.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Agar,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/CCAR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1535-7163
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pubmed:author |
pubmed-author:AboukameelAmroA,
pubmed-author:AdsayVolkanV,
pubmed-author:DuJianhuaJ,
pubmed-author:HatfieldJames SJS,
pubmed-author:KouM TMT,
pubmed-author:LeviEdiE,
pubmed-author:MajumdarAdhip P NAP,
pubmed-author:MajumderPralayP,
pubmed-author:MohammadRamziR,
pubmed-author:RishiArun KAK,
pubmed-author:WaliAnilA,
pubmed-author:YuYingjieY,
pubmed-author:ZhangLiyueL
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pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1661-72
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17513614-Agar,
pubmed-meshheading:17513614-Animals,
pubmed-meshheading:17513614-Antineoplastic Agents,
pubmed-meshheading:17513614-Apoptosis Regulatory Proteins,
pubmed-meshheading:17513614-Breast Neoplasms,
pubmed-meshheading:17513614-Cell Cycle Proteins,
pubmed-meshheading:17513614-Cell Line, Tumor,
pubmed-meshheading:17513614-Cell Proliferation,
pubmed-meshheading:17513614-Female,
pubmed-meshheading:17513614-Gene Silencing,
pubmed-meshheading:17513614-Green Fluorescent Proteins,
pubmed-meshheading:17513614-Humans,
pubmed-meshheading:17513614-Mice,
pubmed-meshheading:17513614-Mice, SCID,
pubmed-meshheading:17513614-Neoplasm Transplantation,
pubmed-meshheading:17513614-Transcriptional Activation
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pubmed:year |
2007
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pubmed:articleTitle |
Transactivator of transcription-tagged cell cycle and apoptosis regulatory protein-1 peptides suppress the growth of human breast cancer cells in vitro and in vivo.
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pubmed:affiliation |
Veterans Affairs Medical Center, Wayne State University, Detroit, Michigan 48201, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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