| pubmed-article:15937546 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15937546 | lifeskim:mentions | umls-concept:C1519346 | lld:lifeskim |
| pubmed-article:15937546 | lifeskim:mentions | umls-concept:C0027627 | lld:lifeskim |
| pubmed-article:15937546 | lifeskim:mentions | umls-concept:C1705165 | lld:lifeskim |
| pubmed-article:15937546 | lifeskim:mentions | umls-concept:C2700061 | lld:lifeskim |
| pubmed-article:15937546 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:15937546 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:15937546 | pubmed:dateCreated | 2005-7-11 | lld:pubmed |
| pubmed-article:15937546 | pubmed:abstractText | In the present study, we demonstrated that human skin cancers frequently overexpress TGF-beta1 but exhibit decreased expression of the TGF-beta type II receptor (TGF-(beta)RII). To understand how this combination affects cancer prognosis, we generated a transgenic mouse model that allowed inducible expression of TGF-beta(1) in keratinocytes expressing a dominant negative TGF-(beta)RII (Delta(beta)RII) in the epidermis. Without Delta(beta)RII expression, TGF-beta1 transgene induction in late-stage, chemically induced papillomas failed to inhibit tumor growth but increased metastasis and epithelial-to-mesenchymal transition (EMT), i.e., formation of spindle cell carcinomas. Interestingly, Delta(beta)RII expression abrogated TGF-beta1-mediated EMT and was accompanied by restoration of membrane-associated E-cadherin/catenin complex in TGF-beta1/Delta(beta)RII compound tumors. Furthermore, expression of molecules thought to mediate TGF-beta1-induced EMT was attenuated in TGF-beta1/Delta(beta)RII-transgenic tumors. However, TGF-beta1/Delta(beta)RII-transgenic tumors progressed to metastasis without losing expression of the membrane-associated E-cadherin/catenin complex and at a rate higher than those observed in nontransgenic, TGF-beta1-transgenic, or Delta(beta)RII-transgenic mice. Abrogation of Smad activation by Delta(beta)RII correlated with the blockade of EMT. However, Delta(beta)RII did not alter TGF-beta1-mediated expression of RhoA/Rac and MAPK, which contributed to increased metastasis. Our study provides evidence that TGF-beta1 induces EMT and invasion via distinct mechanisms. TGF-beta1-mediated EMT requires functional TGF-(beta)RII, whereas TGF-beta1-mediated tumor invasion cooperates with reduced TGF-(beta)RII signaling in tumor epithelia. | lld:pubmed |
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| pubmed-article:15937546 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15937546 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15937546 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15937546 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:15937546 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:BiY HYH | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:WangXiao-Jing... | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:CorlessChrist... | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:Kulesz-Martin... | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:LiAllen GAG | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:HanGangwenG | lld:pubmed |
| pubmed-article:15937546 | pubmed:author | pubmed-author:LuShi-LongSL | lld:pubmed |
| pubmed-article:15937546 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15937546 | pubmed:volume | 115 | lld:pubmed |
| pubmed-article:15937546 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15937546 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15937546 | pubmed:pagination | 1714-23 | lld:pubmed |
| pubmed-article:15937546 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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