ArticleOncogene2007
Blockage of intermediate-conductance-Ca(2+) -activated K(+) channels inhibits progression of human endometrial cancer.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 107 citations in OpenAlex.
- Potassium channels in cancer: from hallmarks to therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Hydrogel-Based Delivery of Ion Channel Modulators for Cancer Therapy: Current Advances and Future Perspectives.Gels (Basel, Switzerland) · 2026Review
- Clotrimazole as a new frontier: Drug repurposing and its efficacy in cancer therapy.Cancer pathogenesis and therapy · 2026Review
- Potassium KCa3.1 channel overexpression deteriorates functionality and availability of channels at the outer cellular membrane.Scientific reports · 2025Article
- Challenges in the Therapeutic Targeting of KCa Channels: From Basic Physiology to Clinical Applications.International journal of molecular sciences · 2024Review
- Overexpression of KCNN4 channels in principal neurons produces an anti-seizure effect without reducing their coding ability.Gene therapy · 2024Article
- IK Channel-Independent Effects of Clotrimazole and Senicapoc on Cancer Cells Viability and Migration.International journal of molecular sciences · 2023Article
- Repurposing antifungal drugs for cancer therapy.Journal of advanced research · 2023Review
- Ion Channels and Personalized Medicine in Gynecological Cancers.Pharmaceuticals (Basel, Switzerland) · 2023Review
- KCNF1 promotes lung cancer by modulating ITGB4 expression.Cancer gene therapy · 2023Article
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- Review
- Ion Channels in Endometrial Cancer.Cancers · 2022Review
- Recent Developments on the Roles of Calcium Signals and Potential Therapy Targets in Cervical Cancer.Cells · 2022Review
- The role of potassium channels in the proliferation and migration of endometrial adenocarcinoma HEC1-A cells.Molecular biology reports · 2022Article
- Quantum Tunneling-Induced Membrane Depolarization Can Explain the Cellular Effects Mediated by Lithium: Mathematical Modeling and Hypothesis.Membranes · 2021Article
- MiR-9-5p Regulates Genes Linked to Cerebral Calcification in the Osteogenic Differentiation Model and Induces Generalized Alteration in the Ion Channels.Journal of molecular neuroscience : MN · 2021Article
- KCNN4 induces multiple chemoresistance in breast cancer by regulating BCL2A1.American journal of cancer research · 2020Article
- MiR-506-3p suppresses the proliferation of ovarian cancer cells by negatively regulating the expression of MTMR6.Journal of biosciences · 2019Article
- KCancers · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Potassium (K(+)) channels have been implicated in proliferation of some tumor cells. However, whether K(+) channels are important to the pathogenesis of endometrial cancer (EC) remains unknown. In the present study, we report that intermediate-conductance Ca(2+)-activated K(+) (IKCa1) channels play a critical role in the development of EC. The expression of IKCa1 at both mRNA and protein levels in EC tissues was greatly increased than that in atypical hyperplasia and normal tissues. Treatment of EC cells with clotrimazole and TRAM-34, two agents known to inhibit IKCa1 channels, suppressed the proliferation of EC cells and blocked EC cell cycle at G(0)/G(1) phase. Similarly, downregulation of IKCa1 by siRNA against IKCa1 inhibited EC cell proliferation and arrested its cell cycle at G(0)/G(1) phase. A clotrimazole-sensitive K(+) current was induced in EC cells in response to the increased Ca(2+). The current density induced by Ca(2+) was greatly reduced by clotrimazole, TRAM-34, charybdotoxin or downregulation of IKCa1 by the siRNA against IKCa1. Furthermore, TRAM-34 and clotrimazole slowed the formation in nude mice of tumor generated by injection of EC cells. Our results suggest that increased activity of IKCa1 channel is necessary for the development of EC.
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Registered trials
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.