Functional expression of mitochondrial KCa3.1 channels in non-small cell lung cancer cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-09-24

AUTHORS

Etmar Bulk, Luca Matteo Todesca, Magdalena Bachmann, Ildiko Szabo, Marius Rieke, Albrecht Schwab

ABSTRACT

Lung cancer is one of the leading causes of cancer-related deaths worldwide. The Ca2+-activated K+ channel KCa3.1 contributes to the progression of non-small cell lung cancer (NSCLC). Recently, KCa3.1 channels were found in the inner membrane of mitochondria in different cancer cells. Mitochondria are the main sources for the generation of reactive oxygen species (ROS) that affect the progression of cancer cells. Here, we combined Western blotting, immunofluorescence, and fluorescent live-cell imaging to investigate the expression and function of KCa3.1 channels in the mitochondria of NSCLC cells. Western blotting revealed KCa3.1 expression in mitochondrial lysates from different NSCLC cells. Using immunofluorescence, we demonstrate a co-localization of KCa3.1 channels with mitochondria of NSCLC cells. Measurements of the mitochondrial membrane potential with TMRM reveal a hyperpolarization following the inhibition of KCa3.1 channels with the cell-permeable blocker senicapoc. This is not the case when cells are treated with the cell-impermeable peptidic toxin maurotoxin. The hyperpolarization of the mitochondrial membrane potential is accompanied by an increased generation of ROS in NSCLC cells. Collectively, our results provide firm evidence for the functional expression of KCa3.1 channels in the inner membrane of mitochondria of NSCLC cells. More... »

PAGES

1147-1157

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00424-022-02748-x

DOI

http://dx.doi.org/10.1007/s00424-022-02748-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1151303310

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/36152073


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