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Trop-2 plasticity is controlled by epithelial-to-mesenchymal transition

J. Remšík, L. Binó, Z. Kahounová, G. Kharaishvili, Š. Šimecková, R. Fedr, T. Kucírková, S. Lenárt, XM. Muresan, E. Slabáková, L. Knopfová, J. Bouchal, M. Král, P. Beneš, K. Soucek,

. 2018 ; 39 (11) : 1411-1418. [pub] 20181213

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc19028321

Grantová podpora
NV15-33999A MZ0 CEP - Centrální evidence projektů
NV15-28628A MZ0 CEP - Centrální evidence projektů

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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$a Remšík, Ján $u Department of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czech Republic. Center of Biomolecular and Cellular Engineering, International Clinical Research Center, St. Anne's University Hospital Brno, Brno, Czech Republic. Department of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
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$a 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.
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