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Bischof, H.* ; Maier, S.* ; Koprowski, P.* ; Kulawiak, B.* ; Burgstaller, S.* ; Jasińska, J.* ; Serafimov, K.* ; Zochowska, M.* ; Gross, D.* ; Schroth, W.* ; Matt, L.* ; Juarez Lopez, D.A.* ; Zhang, Y.* ; Bonzheim, I.* ; Büttner, F.A.* ; Fend, F.* ; Schwab, M.* ; Birkenfeld, A.L. ; Malli, R.* ; Lämmerhofer, M.* ; Bednarczyk, P.* ; Szewczyk, A.* ; Lukowski, R.*

mitoBKCa is functionally expressed in murine and human breast cancer cells and potentially contributes to metabolic reprogramming.

eLife 12:31 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Alterations in the function of K+ channels such as the voltage- and Ca2+-activated K+ channel of large conductance (BKCa) reportedly promote breast cancer (BC) development and progression. Underlying molecular mechanisms remain, however, elusive. Here, we provide electrophysiological evidence for a BKCa splice variant localized to the inner mitochondrial membrane of murine and human BC cells (mitoBKCa). Through a combination of genetic knockdown and knockout along with a cell permeable BKCa channel blocker, we show that mitoBKCa modulates overall cellular and mitochondrial energy production, and mediates the metabolic rewiring referred to as the 'Warburg effect', thereby promoting BC cell proliferation in the presence and absence of oxygen. Additionally, we detect mitoBKCa and BKCa transcripts in low or high abundance, respectively, in clinical BC specimens. Together, our results emphasize, that targeting mitoBKCa could represent a treatment strategy for selected BC patients in future.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter K+ Channels ; Kcnma1 ; Slo1 ; Warburg Effect ; Biosensors ; Breast Cancer ; Cancer Biology ; Cell Biology ; Human ; Metabolic Reprogramming ; Mitobkca ; Mouse; Ca2+-activated K+ Channels; Inner Mitochondrial-membrane; Potassium Channel; Bk Channels; Calcium; Ca2+; Activation; Indicators
ISSN (print) / ISBN 2050-084X
e-ISSN 2050-084X
Zeitschrift eLife
Quellenangaben Band: 12, Heft: , Seiten: , Artikelnummer: 31 Supplement: ,
Verlag eLife Sciences Publications
Verlagsort Sheraton House, Castle Park, Cambridge, Cb3 0ax, England
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)
Förderungen Robert Bosch Stiftung
Interfaculty Centre for Pharmacogenomics and Pharma Research
Austrian Science Fund
Fritz Thyssen Stiftung
Narodowe Centrum Nauki
Deutsche Forschungsgemeinschaft Germany's Excellence Strategy
Deutsche Forschungsgemeinschaft