| pubmed-article:18622428 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18622428 | lifeskim:mentions | umls-concept:C0242275 | lld:lifeskim |
| pubmed-article:18622428 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:18622428 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:18622428 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:18622428 | pubmed:issue | 47 | lld:pubmed |
| pubmed-article:18622428 | pubmed:dateCreated | 2008-10-16 | lld:pubmed |
| pubmed-article:18622428 | pubmed:abstractText | The epidermal growth factor receptor (EGFR) is frequently overexpressed in various tumours of epidermal origin and is held responsible for tumourigenicity and tumour persistence. Increased nuclear factor (NF)-kappaB activity has been suggested to be involved in the malignant behaviour of EGFR-overexpressing cells. However, the mechanisms that regulate EGF-induced NF-kappaB activation are still largely unknown. Here we show that EGF can induce NF-kappaB-dependent gene expression independently from IkappaBalpha degradation or p100 processing in EGFR-overexpressing HEK293T cells. Moreover, EGF-induced NF-kappaB activation could be inhibited by overexpression of ABINs, which were previously identified as intracellular inhibitors of tumour necrosis factor, interleukin-1 and lipopolysaccharide-induced NF-kappaB activation. Knockdown of ABIN-1 by RNA interference boosted the NF-kappaB response upon EGF stimulation. The C-terminal ubiquitin-binding domain containing region of ABINs was crucial and sufficient for NF-kappaB inhibition. Adenoviral gene transfer of ABINs reduced constitutive NF-kappaB activity as well as the proliferation of EGFR-overexpressing A431 and DU145 human carcinoma cells. Altogether, these results demonstrate an important role for an ABIN-sensitive non-classical NF-kappaB signalling pathway in the proliferation of EGFR-overexpressing tumour cells, and indicate a potential use for ABIN gene therapy in the treatment of cancer. | lld:pubmed |
| pubmed-article:18622428 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18622428 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18622428 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18622428 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18622428 | pubmed:issn | 1476-5594 | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:De... | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:HuangLL | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:BeyaertRR | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:RevettKK | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:HeyninckKK | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:WullaertAA | lld:pubmed |
| pubmed-article:18622428 | pubmed:author | pubmed-author:VerstrepenLL | lld:pubmed |
| pubmed-article:18622428 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18622428 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:18622428 | pubmed:volume | 27 | lld:pubmed |
| pubmed-article:18622428 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18622428 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18622428 | pubmed:pagination | 6131-40 | lld:pubmed |
| pubmed-article:18622428 | pubmed:dateRevised | 2010-9-10 | lld:pubmed |
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| pubmed-article:18622428 | pubmed:meshHeading | pubmed-meshheading:18622428... | lld:pubmed |
| pubmed-article:18622428 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18622428 | pubmed:articleTitle | ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells. | lld:pubmed |
| pubmed-article:18622428 | pubmed:affiliation | Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium. | lld:pubmed |
| pubmed-article:18622428 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18622428 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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