ArticleMolecular and cellular biochemistry2002
Inhibitory effects of extracellular Mg2+ on intracellular Ca2+ dynamic changes and thapsigargin-induced apoptosis in human cancer MCF7 cells.
Article in Molecular and cellular biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular Dynamics Simulation of Passive Diffusion across a Human Breast Cancer Cell Membrane Model. Comparison between Cisplatin and Its Pt(IV) Derivatives.Journal of chemical information and modeling · 2026Article
- Optimizing an Osteosarcoma-Fibroblast Coculture Model to Study Antitumoral Activity of Magnesium-Based Biomaterials.International journal of molecular sciences · 2020Article
- G-Protein-Coupled Estrogen Receptor (GPER)-Specific Agonist G1 Induces ER Stress Leading to Cell Death in MCF-7 Cells.Biomolecules · 2019Article
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- The anti-apoptotic effect of regucalcin is mediated through multisignaling pathways.Apoptosis : an international journal on programmed cell death · 2013Review
- Crown Ether Host-Rotaxanes as Cytotoxic Agents.ACS medicinal chemistry letters · 2013Article
- Regucalcin and cell regulation: role as a suppressor protein in signal transduction.Molecular and cellular biochemistry · 2011Review
- Novel protein RGPR-p117: its role as the regucalcin gene transcription factor.Molecular and cellular biochemistry · 2009Review
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The effects of extracellular Mg2+ on both dynamic changes of [Ca2+]i and apoptosis rate were analysed. The consequences of spatial and temporal dynamic changes of intracellular Ca2+ on apoptosis, in thapsigargin- and the calcium-ionophore 4BrA23187-treated MCF7 cells were first determined. Both 4BrA23187 and thapsigargin induced an instant increase of intracellular Ca2+ concentrations ([Ca2+]i) which remained quite elevated (> 150 nM) and lasted for several hours. [Ca2+]i increases were equivalent in the cytosol and the nucleus. The treatments that induced apoptosis in MCF7 cells were systematically associated with high and sustained [Ca2+]i (150 nM) for several hours. The initial [Ca2+]i increase was not determinant in the events triggering apoptosis. Thapsigargin-mediated apoptosis and [Ca2+]i rise were abrogated when cells were pretreated with the calcium chelator BAPTA. The role of the extracellular Mg2+ concentration has been studied in thapsigargin treated cells. High (10 mM) extracellular Mg2+, caused an increase in basal [Mg2+]i from 0.8+/-0.3 to 1.6+/-0.5 mM. As compared to 1.4 mM extracellular Mg2+, 1 microM thapsigargin induces, in 10 mM Mg2+, a reduced percentage from 22 to 11% of fragmented nuclei, a lower sustained [Ca2+]i and a lower Ca2+ influx through the plasma membrane. In conclusion, the cell death induced by thapsigargin was dependent on high and sustained [Ca2+]i which was inhibited by high extracellular and intracellular Mg2+.
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