ArticlePloS one2016
Identification of KCa3.1 Channel as a Novel Regulator of Oxidative Phosphorylation in a Subset of Pancreatic Carcinoma Cell Lines.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- Comparative Interactome Analysis Reveals Architectural Principles Governing KInternational journal of molecular sciences · 2026Article
- pH-Dependent Microenvironmental Ionic Signaling in Pancreatic Ductal Adenocarcinoma.Acta physiologica (Oxford, England) · 2026Review
- Genetic silencing of KChannels (Austin, Tex.) · 2025Article
- The Kv10.1 potassium channel, driver of hypoxia-induced EMT and breast cancer cell aggressiveness.Cancer cell international · 2025Article
- Intermediate Conductance Calcium-Dependent Potassium Channel (KJournal of cellular physiology · 2025Article
- Review
- IK Channel-Independent Effects of Clotrimazole and Senicapoc on Cancer Cells Viability and Migration.International journal of molecular sciences · 2023Article
- Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells.International journal of molecular sciences · 2023Review
- Functional expression of mitochondrial KPflugers Archiv : European journal of physiology · 2022Article
- IKCell death & disease · 2022Article
- KCNN4 Promotes the Stemness Potentials of Liver Cancer Stem Cells by Enhancing Glucose Metabolism.International journal of molecular sciences · 2022Article
- Alternative Targets for Modulators of Mitochondrial Potassium Channels.Molecules (Basel, Switzerland) · 2022Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Current Challenges of Mitochondrial Potassium Channel Research.Frontiers in physiology · 2022Review
- The feeding behaviour of Amyotrophic Lateral Sclerosis mouse models is modulated by the CaBritish journal of pharmacology · 2021Article
- Therapeutic resistance in pancreatic ductal adenocarcinoma: Current challenges and future opportunities.World journal of gastroenterology · 2021Review
- From OCR and ECAR to energy: Perspectives on the design and interpretation of bioenergetics studies.The Journal of biological chemistry · 2021Review
- TRPM2 Oxidation Activates Two Distinct Potassium Channels in Melanoma Cells through Intracellular Calcium Increase.International journal of molecular sciences · 2021Article
- Ethyl isopropyl amiloride decreases oxidative phosphorylation and increases mitochondrial fusion in clonal untransformed and cancer cells.American journal of physiology. Cell physiology · 2021Article
- Targeting mitochondrial ion channels for cancer therapy.Redox biology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) represents the most common form of pancreatic cancer with rising incidence in developing countries and overall 5-year survival rates of less than 5%. The most frequent mutations in PDAC are gain-of-function mutations in KRAS as well as loss-of-function mutations in p53. Both mutations have severe impacts on the metabolism of tumor cells. Many of these metabolic changes are mediated by transporters or channels that regulate the exchange of metabolites and ions between the intracellular compartment and the tumor microenvironment. In the study presented here, our goal was to identify novel transporters or channels that regulate oxidative phosphorylation (OxPhos) in PDAC in order to characterize novel potential drug targets for the treatment of these cancers. We set up a Seahorse Analyzer XF based siRNA screen and identified previously described as well as novel regulators of OxPhos. The siRNA that resulted in the greatest change in cellular oxygen consumption was targeting the KCNN4 gene, which encodes for the Ca2+-sensitive K+ channel KCa3.1. This channel has not previously been reported to regulate OxPhos. Knock-down experiments as well as the use of a small molecule inhibitor confirmed its role in regulating oxygen consumption, ATP production and cellular proliferation. Furthermore, PDAC cell lines sensitive to KCa3.1 inhibition were shown to express the channel protein in the plasma membrane as well as in the mitochondria. These differences in the localization of KCa3.1 channels as well as differences in the regulation of cellular metabolism might offer opportunities for targeted therapy in subsets of PDAC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.