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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Schratter, G; Scheruebel, S; Langthaler, S; Ester, K; Pelzmann, B; Ghaffari-Tabrizi-Wizsy, N; Rezania, S; Gorischek, A; Platzer, D; Zorn-Pauly, K; Ahammer, H; Prokesch, A; Stanzer, S; Devaney, TTJ; Schmidt, K; Jahn, SW; Prassl, R; Bauernhofer, T; Schreibmayer, W; .
GIRK1 triggers multiple cancer-related pathways in the benign mammary epithelial cell line MCF10A.
SCI REP. 2019; 9: 19277 Doi: 10.1038/s41598-019-55683-w [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Führende Autor*innen der Med Uni Graz
Schratter Gebhard
Schreibmayer Wolfgang
Co-Autor*innen der Med Uni Graz
Ahammer Helmut
Bauernhofer Thomas
DeVaney Trevor
Ghaffari Tabrizi-Wizsy Nassim
Gorischek Astrid
Jahn Stephan
Pelzmann Brigitte
Platzer Dieter
Prassl Ruth
Prokesch Andreas
Rezania Simin
Scherübel-Posch Susanne
Stanzer Stefanie
Zorn-Pauly Klaus

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Excessive expression of subunit 1 of GIRK1 in ER+ breast tumors is associated with reduced survival times and increased lymph node metastasis in patients. To investigate possible tumor-initiating properties, benign MCF10A and malign MCF7 mammary epithelial cells were engineered to overexpress GIRK1 neoplasia associated vital parameters and resting potentials were measured and compared to controls. The presence of GIRK1 resulted in resting potentials negative to the controls. Upon GIRK1 overexpression, several cellular pathways were regulated towards pro-tumorigenic action as revealed by comparison of transcriptomes of MCF10AGIRK1 with the control (MCF10AeGFP). According to transcriptome analysis, cellular migration was promoted while wound healing and extracellular matrix interactions were impaired. Vital parameters in MCF7 cells were affected akin the benign MCF10A lines, but to a lesser extent. Thus, GIRK1 regulated cellular pathways in mammary epithelial cells are likely to contribute to the development and progression of breast cancer.

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