ArticleInternational journal of molecular sciences2014
Caveolin-1 limits the contribution of BKCa channel to MCF-7 breast cancer cell proliferation and invasion.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- The progression of triple-negative breast cancer is linked to a gradual decrease of the BK channel in the plasma membrane and an increase in intracellular structures.Pflugers Archiv : European journal of physiology · 2026Article
- Inhibition of cancerous properties of triple-negative MDA-MB-436 cells by targeting the KJournal of physiology and biochemistry · 2025Article
- Review
- A systems biology approach to unveil shared therapeutic targets and pathological pathways across major human cancers.Computational and structural biotechnology journal · 2025Article
- Caveolin-1 knockout mitigates breast cancer metastasis to the lungs via integrin α3 dysregulation in 4T1-induced syngeneic breast cancer model.Cancer gene therapy · 2024Article
- Role of Caveolae family-related proteins in the development of breast cancer.Frontiers in molecular biosciences · 2023Review
- Molecular and Immunohistochemical Alterations in Breast Cancer Patients in Upper Egypt.Reports of biochemistry & molecular biology · 2023Article
- Salinomycin as a potent anticancer stem cell agent: State of the art and future directions.Medicinal research reviews · 2022Review
- Potassium Channels as a Target for Cancer Therapy: Current Perspectives.OncoTargets and therapy · 2022Review
- Caveolin1: its roles in normal and cancer stem cells.Journal of cancer research and clinical oncology · 2021Review
- Identification of Novel MeCP2 Cancer-Associated Target Genes and Post-Translational Modifications.Frontiers in oncology · 2020Article
- Voltage-Gated KFrontiers in pharmacology · 2020Review
- Caveolin-1: a multifaceted driver of breast cancer progression and its application in clinical treatment.OncoTargets and therapy · 2019Review
- CD44 Expression Predicts Prognosis of Ovarian Cancer Patients Through Promoting Epithelial-Mesenchymal Transition (EMT) by Regulating Snail, ZEB1, and Caveolin-1.Frontiers in oncology · 2019Article
- BKCa participates in E2 inducing endometrial adenocarcinoma by activating MEK/ERK pathway.BMC cancer · 2018Article
- HN1 contributes to migration, invasion, and tumorigenesis of breast cancer by enhancing MYC activity.Molecular cancer · 2017Article
- Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention.Oxidative medicine and cellular longevity · 2017Review
- The different functions and clinical significances of caveolin-1 in human adenocarcinoma and squamous cell carcinoma.OncoTargets and therapy · 2017Review
- BKCa promotes growth and metastasis of prostate cancer through facilitating the coupling between αvβ3 integrin and FAK.Oncotarget · 2016Article
- Caveolin-1 overexpression in benign and malignant salivary gland tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that caveolin-1 and large conductance Ca²⁺-activated potassium (BKCa) channels are implicated in the carcinogenesis processes, including cell proliferation and invasion. These two proteins have been proven to interact with each other in vascular endothelial and smooth muscle cells and modulate vascular contractility. In this study, we investigated the probable interaction between caveolin-1 and BKCa in MCF-7 breast cancer cells. We identified that caveolin-1 and BKCa were co-localized and could be reciprocally co-immunoprecipitated in human breast cancer MCF-7 cells. siRNA mediated caveolin-1 knockdown resulted in activation and increased surface expression of BKCa channel, and subsequently promoted the proliferation and invasiveness of breast cancer cells. These effects were attenuated in the presence of BKCa-siRNA. Conversely, up-regulated caveolin-1 suppressed function and surface expression of BKCa channel and exerted negative effects on breast cancer cell proliferation and invasion. Similarly, these opposing effects were abrogated by BKCa up-regulation. Collectively, our findings suggest that BKCa is a critical target for suppression by caveolin-1 in suppressing proliferation and invasion of breast cancer cells. The functional complex of caveolin-1 and BKCa in the membrane microdomain may be served as a potential therapeutic target in breast cancer.
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