GSE138155
GIRK1 triggers multiple cancer-related pathways in the benign mammary epithelial cell line MCF10A
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 overexpressing GIRK1 were engineered, neoplasia associated vital parameters and resting potentials were measured and compared to controls.  Presence of GIRK1 resulted in resting potentials negative to controls. Upon GIRK1 overexpression, several cellular pathways were sizably regulated towards pro-tumorigenic action as revealed by comparison of transcriptomes of MCF10AGIRK1 with 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, although to a lesser extent. Thus, GIRK1 overexpression will aid in classification of ER+ breast tumors and bears the potential to open a new window for the therapy of this detrimental disease. Overall design: Transcriptomes of two MCF10A cell lines stably overexpressing KCNJ3 (GIRK1) and of two control MCF10A lines were assesed