ArticleThe Journal of membrane biology2010
Intermediate Ca2+-sensitive K+ channels are necessary for prolactin-induced proliferation in breast cancer cells.
Article in The Journal of membrane biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting the JAK/STAT pathway in solid tumors.Journal of cancer metastasis and treatment · 2020Article
- SK4 channels modulate CaMolecular oncology · 2017Article
- MICU1 drives glycolysis and chemoresistance in ovarian cancer.Nature communications · 2017Article
- Intermediate-Conductance-Ca2-Activated K Channel IKCa1 Is Upregulated and Promotes Cell Proliferation in Cervical CancerMedical science monitor basic research · 2017Article
- Zinc transporters and dysregulated channels in cancers.Frontiers in bioscience (Landmark edition) · 2017Review
- miR-497-5p inhibits cell proliferation and invasion by targeting KCa3.1 in angiosarcoma.Oncotarget · 2016Article
- Functional cooperation between KCa3.1 and TRPC1 channels in human breast cancer: Role in cell proliferation and patient prognosis.Oncotarget · 2016Article
- Downregulation of the Ca(2+)-activated K(+) channel KC a3.1 by histone deacetylase inhibition in human breast cancer cells.Pharmacology research & perspectives · 2016Article
- X-ray irradiation activates K+ channels via H2O2 signaling.Scientific reports · 2015Article
- The roles of K(+) channels in cancer.Nature reviews. Cancer · 2014Review
- Article
- K(+) channels and cell cycle progression in tumor cells.Frontiers in physiology · 2013Article
- Prolactin induces a hyperpolarising current in rat paraventricular oxytocinergic neurones.Journal of neuroendocrinology · 2011Article
- Calcium-activated K+ channels increase cell proliferation independent of K+ conductance.American journal of physiology. Cell physiology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prolactin (PRL) is a polypeptidic hormone which acts both systemically and locally to cause lactation by interacting with the PRL receptor, a Janus kinase (JAK2)-coupled cytokine receptor family member. Several studies have reported that serum PRL level elevation is associated with an increased risk for breast cancer, and evidence has suggested that PRL is one actor in the pathogenesis and progression of this cancer. We previously reported the involvement of hIKCa1 in breast cell cycle progression and cell proliferation. However, mechanisms by which PRL cooperates with these channels to modulate breast epithelial cell proliferation remain unknown. Our results showed that, in the MCF-7 breast cancer cell line, PRL increased hIKCa1 current density. These channels were functional and regulated the resting membrane potential. The PRL effects were inhibited by TRAM-34 and clotrimazole, the most used hIKCa1 blockers. Moreover, PRL increased proliferation in a dose-dependent manner without overexpressing hIKCa1. To determine whether PRL-induced proliferation and hIKCa1 activity involved the JAK2 pathway, we used pharmacological JAK2 inhibitors (AG490 and JAK inhibitor I). Indeed, PRL-induced JAK2 phosphorylation was required for both cell proliferation and hIKCa1 activity. In the presence of either hIKCa1 blockers or siRNA-hIKCa1, PRL failed to increase cell proliferation and hIKCa1 activity. Taken together, our results demonstrate that PRL plays a role in breast cancer cell proliferation by increasing hIKCa1 activity through the JAK2 signaling pathway.
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