ArticleFEBS letters2012
Subsets of ATP-sensitive potassium channel (KATP) inhibitors increase gap junctional intercellular communication in metastatic cancer cell lines independent of SUR expression.
Article in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Anti-invasive effects of minoxidil on human breast cancer cells: combination with ranolazine.Clinical & experimental metastasis · 2022Article
- Curcumin and Gastric Cancer: a Review on Mechanisms of Action.Journal of gastrointestinal cancer · 2019Review
- Ion-Switchable Quantum Dot Förster Resonance Energy Transfer Rates in Ratiometric Potassium Sensors.ACS nano · 2016Article
- Cyclooxygenase inhibitor induces the upregulation of connexin-43 expression in C6 glioma cells.Biomedical reports · 2016Article
- Ocular Hypotensive Effects of the ATP-Sensitive Potassium Channel Opener Cromakalim in Human and Murine Experimental Model Systems.PloS one · 2015Article
- Curcumin inhibits proliferation of gastric cancer cells by impairing ATP-sensitive potassium channel opening.World journal of surgical oncology · 2014Article
- Glibenclamide inhibits cell growth by inducing G0/G1 arrest in the human breast cancer cell line MDA-MB-231.BMC pharmacology & toxicology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Gap junctional intercellular communication (GJIC) regulates cellular homeostasis by propagating signaling molecules, exchanging cellular metabolites, and coupling electrical signals. In cancer, cells exhibit altered rates of GJIC which may play a role in neoplastic progression. K(ATP) channels help maintain membrane polarity and linkages between K(ATP) channel activity and rates of GJIC have been established. The mechanistic relationship has not been fully elucidated. We report the effects of treatment with multiple K(ATP) antagonist compounds on GJIC in metastatic cell lines demonstrating an increase in communication rates following treatment with compounds possessing specificities towards the SUR2 subunit of K(ATP). These effects remained consistent using cell lines with different expression levels of SUR1 and SUR2, suggesting possible off target effects on GJIC by these compounds.
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Registered trials
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