Oncotarget

Research Papers:

TGF-β inducible epithelial-to-mesenchymal transition in renal cell carcinoma

Sandy Tretbar _, Peter Krausbeck, Anja Müller, Michael Friedrich, Christoforos Vaxevanis, Juergen Bukur, Simon Jasinski-Bergner and Barbara Seliger

PDF  |  Full Text  |  Supplementary Files  |  How to cite

Oncotarget. 2019; 10:1507-1524. https://doi.org/10.18632/oncotarget.26682

Metrics: PDF 1687 views  |   Full Text 3471 views  |   ?  


Abstract

Sandy Tretbar1,*, Peter Krausbeck1,2,*, Anja Müller1, Michael Friedrich1, Christoforos Vaxevanis1, Juergen Bukur1, Simon Jasinski-Bergner1 and Barbara Seliger1

1Martin Luther University Halle-Wittenberg, Institute for Medical Immunology, 06112 Halle, Germany

2State Hospital, Healthcare Centre Glantal, 55590 Meisenheim, Germany

*These authors contributed equally to this work

Correspondence to:

Barbara Seliger, email: [email protected]

Keywords: epithelial-to-mesenchymal transition; renal cell carcinoma; TGF-β; Smad-signaling pathway; inhibition

Received: September 21, 2018     Accepted: February 01, 2019     Published: February 19, 2019

ABSTRACT

Epithelial-to-mesenchymal transition (EMT) is a crucial step in cancer progression and the number one reason for poor prognosis and worse overall survival of patients. Although this essential process has been widely studied in many solid tumors as e.g. melanoma and breast cancer, more detailed research in renal cell carcinoma (RCC) is required, especially for the major EMT-inducer transforming growth factor beta (TGF-β). Here, we provide a study of six different RCC cell lines of two different RCC subtypes and their response to recombinant TGF-β1 treatment. We established a model system shifting the cells to a mesenchymal cell type without losing their mesenchymal character even in the absence of the external stimulus. This model system forms a solid basis for future studies of the EMT process in RCCs to better understand the molecular basis of this process responsible for cancer progression.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 26682