| pubmed-article:16959844 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16959844 | lifeskim:mentions | umls-concept:C0007115 | lld:lifeskim |
| pubmed-article:16959844 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:16959844 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:16959844 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:16959844 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:16959844 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:16959844 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:16959844 | pubmed:dateCreated | 2006-11-19 | lld:pubmed |
| pubmed-article:16959844 | pubmed:abstractText | The BRAFV600E mutation is closely linked to tumorigenesis and malignant phenotype of papillary thyroid cancer. Signaling pathways activated by BRAFV600E are still unclear except a common activation pathway, MAPK cascade. To investigate the possible target of BRAFV600E, we developed two different cell culture models: 1) doxycycline-inducible BRAFV600E-expressing clonal line derived from human thyroid cancer WRO cells originally harboring wild-type BRAF; 2) WRO, KTC-3, and NPA cells infected with an adenovirus vector carrying BRAFV600E. BRAFV600E expression induced ERK phosphorylation and cyclin D1 expression in these cells. The BRAFV600E-overexpressing cells also showed an increase of nuclear factor kappaB (NF-kappaB) DNA-binding activity, resulting in up-regulation of antiapoptotic c-IAP-1, c-IAP-2, and X-linked inhibitor of apoptosis. Furthermore, BRAFV600E expression also induced the expression of matrix metalloproteinase and cell invasion into matrigel through NF-kappaB pathway. Increased invasive ability by BRAFV600E expression was significantly inhibited by a specific NF-kappaB inhibitor, racemic dehydroxymethylepoxyquinomicin. These data indicate that BRAFV600E activates not only MAPK but also NF-kappaB signaling pathway in human thyroid cancer cells, leading to an acquisition of apoptotic resistance and promotion of invasion. Inactivation of NF-kappaB may provide a new therapeutic modality for thyroid cancers with BRAFV600E. | lld:pubmed |
| pubmed-article:16959844 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16959844 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16959844 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16959844 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16959844 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16959844 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:16959844 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:OhtsuruAkiraA | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:YamashitaShun... | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:UmezawaKazuoK | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:NagayamaYujiY | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:NambaHiroyuki... | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:MitsutakeNori... | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:PodtchekoAlex... | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:SaenkoVladimi... | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:SedliarouIlya... | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:PalonaIrynaI | lld:pubmed |
| pubmed-article:16959844 | pubmed:author | pubmed-author:StarenkiDmytr... | lld:pubmed |
| pubmed-article:16959844 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16959844 | pubmed:volume | 147 | lld:pubmed |
| pubmed-article:16959844 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16959844 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16959844 | pubmed:pagination | 5699-707 | lld:pubmed |
| pubmed-article:16959844 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16959844 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16959844 | pubmed:articleTitle | BRAFV600E promotes invasiveness of thyroid cancer cells through nuclear factor kappaB activation. | lld:pubmed |
| pubmed-article:16959844 | pubmed:affiliation | Department of Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki University Hospital, 852-8523, Japan. | lld:pubmed |
| pubmed-article:16959844 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16959844 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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