Trop-2 plasticity is controlled by epithelial-to-mesenchymal transition
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30010814
DOI
10.1093/carcin/bgy095
PII: 5054274
Knihovny.cz E-resources
- MeSH
- Antigens, Neoplasm genetics metabolism MeSH
- Antigens, CD biosynthesis MeSH
- Epithelial-Mesenchymal Transition physiology MeSH
- Epithelial Cells metabolism MeSH
- Cadherins biosynthesis MeSH
- Carcinoma pathology MeSH
- Humans MeSH
- DNA Methylation genetics MeSH
- Cell Adhesion Molecules genetics metabolism MeSH
- Mice, Inbred BALB C MeSH
- Mice MeSH
- Cell Line, Tumor MeSH
- Prostatic Neoplasms mortality pathology MeSH
- Breast Neoplasms mortality pathology MeSH
- Disease Progression MeSH
- Xenograft Model Antitumor Assays MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antigens, Neoplasm MeSH
- Antigens, CD MeSH
- CDH1 protein, human MeSH Browser
- Cadherins MeSH
- Cell Adhesion Molecules MeSH
- TACSTD2 protein, human MeSH Browser
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.
References provided by Crossref.org
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