ArticleMolecular and cellular biochemistry2010
ERK activation and cell growth require CaM kinases in MCF-7 breast cancer cells.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- Changes in the Acetylcholinesterase Enzymatic Activity in Tumor Development and Progression.Cancers · 2023Review
- The mitochondrial regulation of smooth muscle cell proliferation in type 2 diabetes.bioRxiv : the preprint server for biology · 2023Article
- Muscarinic Receptors Associated with Cancer.Cancers · 2022Review
- The molecular mechanism of chronic stress affecting the occurrence and development of breast cancer and potential drug therapy.Translational oncology · 2022Review
- Investigation of the effects of overexpression of jumping translocation breakpoint (JTB) protein in MCF7 cells for potential use as a biomarker in breast cancer.American journal of cancer research · 2022Article
- Hinge Binder Scaffold Hopping Identifies Potent Calcium/Calmodulin-Dependent Protein Kinase Kinase 2 (CAMKK2) Inhibitor Chemotypes.Journal of medicinal chemistry · 2021Article
- Review
- In Depth Analysis of Kinase Cross Screening Data to Identify CAMKK2 Inhibitory Scaffolds.Molecules (Basel, Switzerland) · 2020Article
- Tissue transglutaminase (TG2) enables survival of human malignant pleural mesothelioma cells in hypoxia.Cell death & disease · 2017Article
- Pleiotropic roles of CaToxicology letters · 2016Article
- Tissue transglutaminase-2 promotes gastric cancer progression via the ERK1/2 pathway.Oncotarget · 2016Article
- Muscarinic receptor M3 mediates cell proliferation induced by acetylcholine and contributes to apoptosis in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- ERp19 contributes to tumorigenicity in human gastric cancer by promoting cell growth, migration and invasion.Oncotarget · 2015Article
- A regulatory feedback loop between Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and the androgen receptor in prostate cancer progression.The Journal of biological chemistry · 2012Article
- Muscarinic receptor agonists and antagonists: effects on cancer.Handbook of experimental pharmacology · 2012Review
- Calmodulin-kinases regulate basal and estrogen stimulated medulloblastoma migration via Rac1.Journal of neuro-oncology · 2011Article
- ER-α36, a novel variant of ER-α, mediates estrogen-stimulated proliferation of endometrial carcinoma cells via the PKCδ/ERK pathway.PloS one · 2010Article
- The RNA binding protein HuR differentially regulates unique subsets of mRNAs in estrogen receptor negative and estrogen receptor positive breast cancer.BMC cancer · 2010Article
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Previous studies on MCF-7 breast cancer cells have shown that the G-protein coupled receptor (GPCR) agonist carbachol increases intracellular calcium levels and the activation of extracellular signal-regulated kinase (ERK). Calcium and calmodulin regulate the calcium/calmodulin-dependent kinase (CaM kinase) family of proteins that have been proposed to regulate ERK and gene transcription. Our results suggest that both estrogen (E2) and carbachol treatment of MCF-7 breast cancer cells trigger phosphorylation of ERK1/2 and the transcription factor Elk-1. Carbachol and estrogen triggered nearly a four- to sixfold increase in MCF-7 cell proliferation by 96 h, respectively. Carbachol-stimulated ERK activation and cell growth was completely blocked by the Muscarinic M(3)-subtype GPCR inhibitor, 4-DAMP, and siRNA against the M(3)-subtype GPCR. Interestingly, blockade of CaM KK with the selective inhibitor STO-609 prevented carbachol activation CaM KI, ERK, Elk-1, and cell growth. Consistent with these observations, knockdown of CaM KKalpha and CaM KIgamma with shRNA-containing plasmids blocked ERK activation by carbachol. In addition, Elk-1 phosphorylation and luciferase activity in response to carbachol treatment was also dependent upon CaM kinases and was inhibited by U0126, STO-609, and siRNA knockdown of CaM kinases and ERK2. Finally, blockade of either CaM KK (with STO-609) or ERK (with U0126) activities resulted in the inhibition of carbachol- and estrogen-mediated cyclin D1 expression and MCF-7 cell growth. Taken together, our results suggest that carbachol treatment of MCF-7 cells activates CaM KI, ERK, the transcription factor Elk-1, cyclin D1, and cell growth through CaM KK.
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