Home
Deutsch
Advanced Search
Browse by ...
Publication overview
Contact persons
Help
Publ. Version/Full Text
Research data
DOI
PMC
 |
Open Access Gold |
|
as soon as is submitted to ZB.
IKCa channels control breast cancer metabolism including AMPK-driven autophagy.
Cell Death Dis. 13:902 (2022)
Ca2+-activated K+ channels of intermediate conductance (IK) are frequently overexpressed in breast cancer (BC) cells, while IK channel depletion reduces BC cell proliferation and tumorigenesis. This raises the question, of whether and mechanistically how IK activity interferes with the metabolic activity and energy consumption rates, which are fundamental for rapidly growing cells. Using BC cells obtained from MMTV-PyMT tumor-bearing mice, we show that both, glycolysis and mitochondrial ATP-production are reduced in cells derived from IK-deficient breast tumors. Loss of IK altered the sub-/cellular K+- and Ca2+- homeostasis and mitochondrial membrane potential, ultimately resulting in reduced ATP-production and metabolic activity. Consequently, we find that BC cells lacking IK upregulate AMP-activated protein kinase activity to induce autophagy compensating the glycolytic and mitochondrial energy shortage. Our results emphasize that IK by modulating cellular Ca2+- and K+-dynamics contributes to the remodeling of metabolic pathways in cancer. Thus, targeting IK channel might disturb the metabolic activity of BC cells and reduce malignancy.
Altmetric
Additional Metrics?
Edit extra informations
Login
Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
2041-4889
e-ISSN
2041-4889
Journal
Cell Death & Disease
Quellenangaben
Volume: 13,
Issue: 10,
Article Number: 902
Publisher
Nature Publishing Group
Non-patent literature
Publications
Reviewing status
Peer reviewed
Grants
Deutsche Forschungsgemeinschaft (German Research Foundation)