ArticleBMC cancer2004
Expression of inwardly rectifying potassium channels (GIRKs) and beta-adrenergic regulation of breast cancer cell lines.
Article in BMC cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- Trial watch: beta-blockers in cancer therapy.Oncoimmunology · 2023Article
- Potassium Channels as a Target for Cancer Therapy: Current Perspectives.OncoTargets and therapy · 2022Review
- Pathological role of ion channels and transporters in the development and progression of triple-negative breast cancer.Cancer cell international · 2020Review
- GIRK1 triggers multiple cancer-related pathways in the benign mammary epithelial cell line MCF10A.Scientific reports · 2019Article
- Overexpression of KCNJ3 gene splice variants affects vital parameters of the malignant breast cancer cell line MCF-7 in an opposing manner.BMC cancer · 2016Article
- Association of adrenergic receptor gene polymorphisms in gallbladder cancer susceptibility in a North Indian population.Journal of cancer research and clinical oncology · 2014Article
- Membrane potential and cancer progression.Frontiers in physiology · 2013Article
- ADRB2 G-G haplotype associated with breast cancer risk among Hispanic and non-Hispanic white women: interaction with type 2 diabetes and obesity.Cancer causes & control : CCC · 2012Article
- Involvement of α2- and β2-adrenoceptors on breast cancer cell proliferation and tumour growth regulation.British journal of pharmacology · 2012Article
- Pancreatic cancer cells and normal pancreatic duct epithelial cells express an autocrine catecholamine loop that is activated by nicotinic acetylcholine receptors α3, α5, and α7.Molecular cancer research : MCR · 2012Article
- Antagonists show GTP-sensitive high-affinity binding to the sigma-1 receptor.British journal of pharmacology · 2011Article
- Beta-adrenergic signaling, a novel target for cancer therapy?Oncotarget · 2010Article
- G-Protein Inwardly Rectifying Potassium Channel 1 (GIRK1) Knockdown Decreases Beta-Adrenergic, MAP Kinase and Akt Signaling in the MDA-MB-453 Breast Cancer Cell Line.Breast cancer : basic and clinical research · 2008Article
- Protein expression of G-protein inwardly rectifying potassium channels (GIRK) in breast cancer cells.BMC physiology · 2006Article
- Expression of G-protein inwardly rectifying potassium channels (GIRKs) in lung cancer cell lines.BMC cancer · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious research has indicated that at various organ sites there is a subset of adenocarcinomas that is regulated by beta-adrenergic and arachidonic acid-mediated signal transduction pathways. We wished to determine if this regulation exists in breast adenocarcinomas. Expression of mRNA that encodes a G-protein coupled inwardly rectifying potassium channel (GIRK1) has been shown in tissue samples from approximately 40% of primary human breast cancers. Previously, GIRK channels have been associated with beta-adrenergic signaling.
methodsBreast cancer cell lines were screened for GIRK channels by RT-PCR. Cell cultures of breast cancer cells were treated with beta-adrenergic agonists and antagonists, and changes in gene expression were determined by both relative competitive and real time PCR. Potassium flux was determined by flow cytometry and cell signaling was determined by western blotting.
resultsBreast cancer cell lines MCF-7, MDA-MB-361 MDA-MB 453, and ZR-75-1 expressed mRNA for the GIRK1 channel, while MDA-MB-468 and MDA-MB-435S did not. GIRK4 was expressed in all six breast cancer cell lines, and GIRK2 was expressed in all but ZR-75-1 and MDA-MB-435. Exposure of MDA-MB-453 cells for 6 days to the beta-blocker propranolol (1 microM) increased the GIRK1 mRNA levels and decreased beta2-adrenergic mRNA levels, while treatment for 30 minutes daily for 7 days had no effect. Exposure to a beta-adrenergic agonist and antagonist for 24 hours had no effect on gene expression. The beta adrenergic agonist, formoterol hemifumarate, led to increases in K+ flux into MDA-MB-453 cells, and this increase was inhibited by the GIRK channel inhibitor clozapine. The tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a high affinity agonist for beta-adrenergic receptors stimulated activation of Erk 1/2 in MDA-MB-453 cells.
conclusionsOur data suggests beta-adrenergic receptors and GIRK channels may play a role in breast cancer.
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