| pubmed-article:18579583 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18579583 | lifeskim:mentions | umls-concept:C0021344 | lld:lifeskim |
| pubmed-article:18579583 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:18579583 | lifeskim:mentions | umls-concept:C0029005 | lld:lifeskim |
| pubmed-article:18579583 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
| pubmed-article:18579583 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:18579583 | pubmed:dateCreated | 2008-8-15 | lld:pubmed |
| pubmed-article:18579583 | pubmed:abstractText | Infection by human papillomavirus (HPV) is a major risk factor for human cervical carcinoma. However, the HPV infection alone is not sufficient for cancer formation. Cervical carcinogenesis is considered a multistep process accompanied by genetic alterations of the cell. Ras is activated in approximately 20% of human cancers, and it is related to the metastatic conversion of tumor cells. We investigated how Ras activation was involved in the malignant conversion of HPV-infected lesions. The active form of H-ras was introduced into human primary keratinocytes expressing the HPV type 18 (HPV18) oncoproteins E6 and/or E7. We analyzed the keratinocytes' growth potentials and found that the activation of the Ras pathway induced senescence-like growth arrest. Senescence could be eliminated by high-risk E7 expression, suggesting that the pRb pathway was important for Ras-induced senescence. Then we analyzed the effect of Ras activation on epidermis development by using an organotypic "raft" culture and found that the E7 and H-ras coexpressions conferred invasive potential on the epidermis. This invasiveness resulted from the upregulation of MT1-MMP and MMP9 by H-ras and E7, respectively, in which the activation of the MEK/extracellular signal-regulated kinase pathway was involved. These results indicated that the activation of Ras or the related signal pathways promoted the malignant conversion of HPV-infected cells. | lld:pubmed |
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| pubmed-article:18579583 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18579583 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18579583 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18579583 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18579583 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:18579583 | pubmed:issn | 1098-5514 | lld:pubmed |
| pubmed-article:18579583 | pubmed:author | pubmed-author:SakaiHiroyuki... | lld:pubmed |
| pubmed-article:18579583 | pubmed:author | pubmed-author:YoshidaSatosh... | lld:pubmed |
| pubmed-article:18579583 | pubmed:author | pubmed-author:NakamuraHiroy... | lld:pubmed |
| pubmed-article:18579583 | pubmed:author | pubmed-author:KajitaniNaoko... | lld:pubmed |
| pubmed-article:18579583 | pubmed:author | pubmed-author:SatsukaAyanoA | lld:pubmed |
| pubmed-article:18579583 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18579583 | pubmed:volume | 82 | lld:pubmed |
| pubmed-article:18579583 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18579583 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18579583 | pubmed:pagination | 8820-7 | lld:pubmed |
| pubmed-article:18579583 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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