Trop-2 plasticity is controlled by epithelial-to-mesenchymal transition
Jazyk angličtina Země Velká Británie, Anglie Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
30010814
DOI
10.1093/carcin/bgy095
PII: 5054274
Knihovny.cz E-zdroje
- MeSH
- antigeny nádorové genetika metabolismus MeSH
- CD antigeny biosyntéza MeSH
- epitelo-mezenchymální tranzice fyziologie MeSH
- epitelové buňky metabolismus MeSH
- kadheriny biosyntéza MeSH
- karcinom patologie MeSH
- lidé MeSH
- metylace DNA genetika MeSH
- molekuly buněčné adheze genetika metabolismus MeSH
- myši inbrední BALB C MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- nádory prostaty mortalita patologie MeSH
- nádory prsu mortalita patologie MeSH
- progrese nemoci MeSH
- xenogenní modely - testy antitumorózní aktivity MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny nádorové MeSH
- CD antigeny MeSH
- CDH1 protein, human MeSH Prohlížeč
- kadheriny MeSH
- molekuly buněčné adheze MeSH
- TACSTD2 protein, human MeSH Prohlížeč
The cell surface glycoprotein Trop-2 is commonly overexpressed in carcinomas and represents an exceptional antigen for targeted therapy. Here, we provide evidence that surface Trop-2 expression is functionally connected with an epithelial phenotype in breast and prostate cell lines and in patient tumor samples. We further show that Trop-2 expression is suppressed epigenetically or through the action of epithelial-to-mesenchymal transition transcription factors and that deregulation of Trop-2 expression is linked with cancer progression and poor patient prognosis. Moreover, our data suggest that the cancer plasticity-driven intratumoral heterogeneity in Trop-2 expression may significantly contribute to response and resistance to therapies targeting Trop-2-expressing cells.
Citace poskytuje Crossref.org
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