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4 results on '"Vandier C"'

1. Ophiobolin A induces paraptosis-like cell death in human glioblastoma cells by decreasing BKCa channel activity.

Author

UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, Bury, M, Girault, A, Mégalizzi, V, Spiegl-Kreinecker, S, Mathieu, V, Berger, W, Evidente, A, Kornienko, A, Gailly, Philippe, Vandier, C, Kiss, R, UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, Bury, M, Girault, A, Mégalizzi, V, Spiegl-Kreinecker, S, Mathieu, V, Berger, W, Evidente, A, Kornienko, A, Gailly, Philippe, Vandier, C, and Kiss, R

Abstract

Glioblastoma multiforme (GBM) is the most lethal and common malignant human brain tumor. The intrinsic resistance of highly invasive GBM cells to radiation- and chemotherapy-induced apoptosis accounts for the generally dismal treatment outcomes. This study investigated ophiobolin A (OP-A), a fungal metabolite from Bipolaris species, for its promising anticancer activity against human GBM cells exhibiting varying degrees of resistance to proapoptotic stimuli. We found that OP-A induced marked changes in the dynamic organization of the F-actin cytoskeleton, and inhibited the proliferation and migration of GBM cells, likely by inhibiting big conductance Ca(2+)-activated K(+) channel (BKCa) channel activity. Moreover, our results indicated that OP-A induced paraptosis-like cell death in GBM cells, which correlated with the vacuolization, possibly brought about by the swelling and fusion of mitochondria and/or the endoplasmic reticulum (ER). In addition, the OP-A-induced cell death did not involve the activation of caspases. We also showed that the expression of BKCa channels colocalized with these two organelles (mitochondria and ER) was affected in this programmed cell death pathway. Thus, this study reveals a novel mechanism of action associated with the anticancer effects of OP-A, which involves the induction of paraptosis through the disruption of internal potassium ion homeostasis. Our findings offer a promising therapeutic strategy to overcome the intrinsic resistance of GBM cells to proapoptotic stimuli.

Published
2013

2. Ophiobolin A induces paraptosis-like cell death in human glioblastoma cells by decreasing BKCa channel activity

Author

Antonio Evidente, Marina Bury, Christophe Vandier, Sabine Spiegl-Kreinecker, Mathieu, Alexander Kornienko, Alban Girault, Robert Kiss, Walter Berger, Mégalizzi, Philippe Gailly, Laboratoire de Toxicologie, Université libre de Bruxelles (ULB), Nutrition, croissance et cancer (U 1069) (N2C), Université de Tours-Institut National de la Santé et de la Recherche Médicale (INSERM), Department f Neurosurgery, Landesnervenklinik Wagner Jauregg Hospital in Linz, Department of Medicine I, Medical University Vienna, Dipartimento di Scienze Chimiche, Università degli studi di Napoli Federico II, Department of Chemistry and Biochemistry, Texas State University, laboratoire de Physiologie Cellulaire, Université Catholique de Louvain = Catholic University of Louvain (UCL), Vandier, Christophe, Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Naples Federico II = Università degli studi di Napoli Federico II, Bury, M., Girault, A., Megalizzi, V., Spiegl-Kreinecker, S., Mathieu, V., Berger, W., Evidente, A., Kornienko, A., Gailly, P., Vandier, C., and Kiss, R.

Subjects
Cancer Research, Patch-Clamp Techniques, Patch-Clamp Technique, Potassium ion homeostasis, Endoplasmic Reticulum, Paraptosis, Membrane Potentials, Antineoplastic Agent, 0302 clinical medicine, Cell Movement, Homeostasis, Large-Conductance Calcium-Activated Potassium Channel alpha Subunits, Caspase, 0303 health sciences, biology, Cell Death, Brain Neoplasms, Ophiobolin A, 3. Good health, Cell biology, Mitochondria, 030220 oncology & carcinogenesis, Original Article, Human, ophiobolin A, Programmed cell death, Sesterterpenes, BKCa channel, Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, Antineoplastic Agents, Paraptosi, Membrane Potential, Brain Neoplasm, 03 medical and health sciences, Cellular and Molecular Neuroscience, Pharmacologie moléculaire et cellulaire, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, Homeostasi, Toxicologie pharmaceutique, Humans, Actin, 030304 developmental biology, Cell Proliferation, Sesterterpene, Cell growth, Endoplasmic reticulum, glioblastoma, Cell Biology, Actins, Cancérologie, Apoptosis, Cell culture, Drug Resistance, Neoplasm, Large-Conductance Calcium-Activated Potassium Channel alpha Subunit, biology.protein, Potassium, paraptosis, Glioblastoma
Abstract

Glioblastoma multiforme (GBM) is the most lethal and common malignant human brain tumor. The intrinsic resistance of highly invasive GBM cells to radiation- and chemotherapy-induced apoptosis accounts for the generally dismal treatment outcomes. This study investigated ophiobolin A (OP-A), a fungal metabolite from Bipolaris species, for its promising anticancer activity against human GBM cells exhibiting varying degrees of resistance to proapoptotic stimuli. We found that OP-A induced marked changes in the dynamic organization of the F-actin cytoskeleton, and inhibited the proliferation and migration of GBM cells, likely by inhibiting big conductance Ca(2+)-activated K(+) channel (BKCa) channel activity. Moreover, our results indicated that OP-A induced paraptosis-like cell death in GBM cells, which correlated with the vacuolization, possibly brought about by the swelling and fusion of mitochondria and/or the endoplasmic reticulum (ER). In addition, the OP-A-induced cell death did not involve the activation of caspases. We also showed that the expression of BKCa channels colocalized with these two organelles (mitochondria and ER) was affected in this programmed cell death pathway. Thus, this study reveals a novel mechanism of action associated with the anticancer effects of OP-A, which involves the induction of paraptosis through the disruption of internal potassium ion homeostasis. Our findings offer a promising therapeutic strategy to overcome the intrinsic resistance of GBM cells to proapoptotic stimuli., Journal Article, Research Support, Non-U.S. Gov't, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2013

3. Ca 2+ protein alpha 1D of CaV1.3 regulates intracellular calcium concentration and migration of colon cancer cells through a non-canonical activity.

Author

Fourbon Y, Guéguinou M, Félix R, Constantin B, Uguen A, Fromont G, Lajoie L, Magaud C, Lecomte T, Chamorey E, Chatelier A, Mignen O, Potier-Cartereau M, Chantôme A, Bois P, and Vandier C

Subjects
Active Transport, Cell Nucleus, Cell Membrane metabolism, Cell Nucleus metabolism, Colonic Neoplasms physiopathology, Cytosol metabolism, Electrophysiological Phenomena, Endoplasmic Reticulum metabolism, Gene Expression Regulation, Neoplastic, HCT116 Cells, Humans, Sodium-Calcium Exchanger metabolism, Calcium metabolism, Calcium Channels, L-Type chemistry, Calcium Channels, L-Type metabolism, Cell Movement, Colonic Neoplasms metabolism, Colonic Neoplasms pathology, Intracellular Space metabolism
Abstract

It is generally accepted that voltage-gated Ca 2+ channels, CaV, regulate Ca 2+ homeostasis in excitable cells following plasma membrane depolarization. Here, we show that the Ca 2+ protein α1D of CaV1.3 channel is overexpressed in colorectal cancer biopsies compared to normal tissues. Gene silencing experiments targeting α1D reduced the migration and the basal cytosolic Ca 2+ concentration of HCT116 colon cancer cell line and modified the cytosolic Ca 2+ oscillations induced by the sodium/calcium exchanger NCX1/3 working in its reverse mode. Interestingly, NCX1/3 regulated membrane potential of HCT116 cells only when α1D was silenced, and blocking NCX1/3 increased cytosolic Ca 2+ concentration and cell migration. However, membrane depolarization did not induce an increase in intracellular Ca 2+ . Patch-clamp experiments clearly showed that the inward Ca 2+ current was absent. Finally, flow cytometry and immunofluorescence studies showed that α1D protein was localized at the plasma membrane, in cytosol and cell nuclei. Altogether, we uncover a novel signaling pathway showing that α1D is involved in the regulation of Ca 2+ homeostasis and cell migration by a mechanism independent of its plasma membrane canonical function but that involved plasma membrane Na + /Ca 2+ exchanger.

Published
2017
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4. The SigmaR1 chaperone drives breast and colorectal cancer cell migration by tuning SK3-dependent Ca 2+ homeostasis.

Author

Gueguinou M, Crottès D, Chantôme A, Rapetti-Mauss R, Potier-Cartereau M, Clarysse L, Girault A, Fourbon Y, Jézéquel P, Guérin-Charbonnel C, Fromont G, Martin P, Pellissier B, Schiappa R, Chamorey E, Mignen O, Uguen A, Borgese F, Vandier C, and Soriani O

Subjects
Breast Neoplasms genetics, Breast Neoplasms mortality, Calcium metabolism, Cell Line, Tumor, Colorectal Neoplasms genetics, Colorectal Neoplasms mortality, Female, Humans, Male, Neoplasm Proteins genetics, ORAI1 Protein genetics, ORAI1 Protein metabolism, Receptors, sigma genetics, Small-Conductance Calcium-Activated Potassium Channels genetics, Sigma-1 Receptor, Breast Neoplasms metabolism, Calcium Signaling, Cell Movement, Colorectal Neoplasms metabolism, Neoplasm Proteins metabolism, Receptors, sigma metabolism, Small-Conductance Calcium-Activated Potassium Channels metabolism
Abstract

The remodeling of calcium homeostasis contributes to the cancer hallmarks and the molecular mechanisms involved in calcium channel regulation in tumors remain to be characterized. Here, we report that SigmaR1, a stress-activated chaperone, is required to increase calcium influx by triggering the coupling between SK3, a Ca 2+ -activated K + channel (KCNN3) and the voltage-independent calcium channel Orai1. We show that SigmaR1 physically binds SK3 in BC cells. Inhibition of SigmaR1 activity, either by molecular silencing or by the use of sigma ligand (igmesine), decreased SK3 current and Ca 2+ entry in breast cancer (BC) and colorectal cancer (CRC) cells. Interestingly, SigmaR1 inhibition diminished SK3 and/or Orai1 levels in lipid nanodomains isolated from BC cells. Analyses of tissue microarray from CRC patients showed higher SigmaR1 expression levels in cancer samples and a correlation with tumor grade. Moreover, the exploration of a cohort of 4937 BC patients indicated that high expression of SigmaR1 and Orai1 channels was significantly correlated to a lower overall survival. As the SK3/Orai1 tandem drives invasive process in CRC and bone metastasis progression in BC, our results may inaugurate innovative therapeutic approaches targeting SigmaR1 to control the remodeling of Ca 2+ homeostasis in epithelial cancers.

Published
2017
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