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2. Senescence Induced by UVB in Keratinocytes Impairs Amino Acids Balance

Author

Bauwens, Emilie, Parée, Tom, Meurant, Sébastien, Bouriez, Inès, Hannart, Clotilde, Wéra, Anne-Catherine, Khelfi, Alexis, Fattaccioli, Antoine, Burteau, Sophie, Demazy, Catherine, Fransolet, Maude, De Schutter, Clémentine, Martin, Nathalie, Théry, Julien, Decanter, Gauthier, Penel, Nicolas, Bury, Marina, Pluquet, Olivier, Garmyn, Marjan, and Debacq-Chainiaux, Florence

Published
2023
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4. Chromatin remodeling regulates catalase expression during cancer cells adaptation to chronic oxidative stress

Author

Glorieux, Christophe, Sandoval, Juan Marcelo, Fattaccioli, Antoine, Dejeans, Nicolas, Garbe, James C, Dieu, Marc, Verrax, Julien, Renard, Patricia, Huang, Peng, and Calderon, Pedro Buc

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Genetics, Prevention, Cancer, Breast Cancer, 1.1 Normal biological development and functioning, Underpinning research, Adaptation, Physiological, Base Sequence, Catalase, Cell Line, Cell Line, Tumor, Chromatin, Chromatin Assembly and Disassembly, Epithelial Cells, Gene Expression Regulation, Neoplastic, Histone Deacetylases, Humans, Hydrogen Peroxide, MCF-7 Cells, Oxidative Stress, Promoter Regions, Genetic, Reactive Oxygen Species, Retinoic Acid Receptor alpha, Signal Transduction, Transcription Factors, Transcription, Genetic, Breast cancer cells, Chromatin remodeling, JunB, Oxidative stress, RARα, Medicinal and Biomolecular Chemistry, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

Regulation of ROS metabolism plays a major role in cellular adaptation to oxidative stress in cancer cells, but the molecular mechanism that regulates catalase, a key antioxidant enzyme responsible for conversion of hydrogen peroxide to water and oxygen, remains to be elucidated. Therefore, we investigated the transcriptional regulatory mechanism controlling catalase expression in three human mammary cell lines: the normal mammary epithelial 250MK primary cells, the breast adenocarcinoma MCF-7 cells and an experimental model of MCF-7 cells resistant against oxidative stress resulting from chronic exposure to H2O2 (Resox), in which catalase was overexpressed. Here we identify a novel promoter region responsible for the regulation of catalase expression at -1518/-1226 locus and the key molecules that interact with this promoter and affect catalase transcription. We show that the AP-1 family member JunB and retinoic acid receptor alpha (RARα) mediate catalase transcriptional activation and repression, respectively, by controlling chromatin remodeling through a histone deacetylases-dependent mechanism. This regulatory mechanism plays an important role in redox adaptation to chronic exposure to H2O2 in breast cancer cells. Our study suggests that cancer adaptation to oxidative stress may be regulated by transcriptional factors through chromatin remodeling, and reveals a potential new mechanism to target cancer cells.

Published
2016

5. Budget‐Friendly Generation, Biochemical Analyses, and Lentiviral Transduction of Patient‐Derived Colon Organoids

Author

Rigaux, Emilie, primary, Chen, Jia‐Wei, additional, George, Fabienne, additional, Lemaire, Julien, additional, Bertrand, Claude, additional, Faugeras, Laurence, additional, Fattaccioli, Antoine, additional, Gilliaux, Quentin, additional, D'Hondt, Lionel, additional, Michiels, Carine, additional, Renard, Henri‐François, additional, and Zanin, Natacha, additional

Published
2023
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6. The global downregulation of protein synthesis observed during hepatogenic maturation is associated with a decrease in TOP mRNA translation

Author

Caruso, Marino, primary, Meurant, Sébastien, additional, Detraux, Damien, additional, Mathieu, Amandine, additional, Gilson, Manon, additional, Dieu, Marc, additional, Fattaccioli, Antoine, additional, Demazy, Catherine, additional, Najimi, Mustapha, additional, Sokal, Etienne, additional, Arnould, Thierry, additional, Verfaillie, Catherine, additional, Lafontaine, Denis L.J., additional, and Renard, Patricia, additional

Published
2023
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7. Senescence Induced by UVB in Keratinocytes Impairs Amino Acids Balance

Author

Bauwens, Emilie, primary, Parée, Tom, additional, Meurant, Sébastien, additional, Bouriez, Inès, additional, Hannart, Clotilde, additional, Wéra, Anne-Catherine, additional, Khelfi, Alexis, additional, Fattaccioli, Antoine, additional, Burteau, Sophie, additional, Demazy, Catherine, additional, Fransolet, Maude, additional, De Schutter, Clémentine, additional, Martin, Nathalie, additional, Théry, Julien, additional, Decanter, Gauthier, additional, Penel, Nicolas, additional, Bury, Marina, additional, Pluquet, Olivier, additional, Garmyn, Marjan, additional, and Debacq-Chainiaux, Florence, additional

Published
2022
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9. The HCV Envelope Glycoprotein Down-Modulates NF-κB Signalling and Associates With Stimulation of the Host Endoplasmic Reticulum Stress Pathway

Author

McKay, Lindsay G. A., primary, Thomas, Jordan, additional, Albalawi, Wejdan, additional, Fattaccioli, Antoine, additional, Dieu, Marc, additional, Ruggiero, Alessandra, additional, McKeating, Jane A., additional, Ball, Jonathan K., additional, Tarr, Alexander W., additional, Renard, Patricia, additional, Pollakis, Georgios, additional, and Paxton, William A., additional

Published
2022
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10. HDAC2 and 7 down-regulation induces senescence in dermal fibroblasts

Author

Warnon, Céline, primary, Bouhjar, Karim, additional, Ninane, Noëlle, additional, Verhoyen, Mathilde, additional, Fattaccioli, Antoine, additional, Fransolet, Maude, additional, Lambert de Rouvroit, Catherine, additional, Poumay, Yves, additional, Piel, Géraldine, additional, Mottet, Denis, additional, and Debacq-Chainiaux, Florence, additional

Published
2021
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11. MPV17 does not control cancer cell proliferation

Author

Canonne, Morgane, Wanet, Anaïs, Nguyen, Thuy Truong An, Khelfi, Alexis, Ayama-Canden, Sophie, Van Steenbrugge, Martine, Fattaccioli, Antoine, Sokal, Etienne, Najimi, Mustapha, Arnould, Thierry, Renard, Patricia, Martin, Negin P., UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, and UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique

Subjects
Proteomics, 0301 basic medicine, Molecular biology, Protein Expression, Gene Expression, Biochemistry, cancer MPV17 shRNA, Sequencing techniques, 0302 clinical medicine, Neoplasms, Enzyme assays, Colorimetric assays, MPV17, Inner mitochondrial membrane, Bioassays and physiological analysis, Gene knockdown, MTT assay, Multidisciplinary, RNA sequencing, Hep G2 Cells, General Medicine, Mitochondrial DNA, Mitochondria, Cell biology, Nucleic acids, Cell Processes, Mitochondrial Membranes, Medicine, General Agricultural and Biological Sciences, Research Article, Forms of DNA, Science, Genetics and Molecular Biology, Biology, DNA, Mitochondrial, Mitochondrial Proteins, 03 medical and health sciences, Extraction techniques, Genetics, Gene Expression and Vector Techniques, medicine, Humans, Gene silencing, Cell Proliferation, Molecular Biology Assays and Analysis Techniques, Cell growth, Membrane Proteins, Biology and Life Sciences, Cell Biology, DNA, medicine.disease, RNA extraction, Research and analysis methods, HEK293 Cells, Molecular biology techniques, 030104 developmental biology, Biochemical analysis, Cancer cell, Mitochondrial DNA depletion syndrome, General Biochemistry, Protein Abundance, 030217 neurology & neurosurgery
Abstract

MPV17 is described as a mitochondrial inner membrane channel. Although its function remains elusive, mutations in the MPV17 gene result in hepato-cerebral mitochondrial DNA depletion syndrome in humans. In this study, we show that MPV17 silencing does not induce depletion in mitochondrial DNA content in cancer cells. We also show that MPV17 does not control cancer cell proliferation despite the fact that we initially observed a reduced proliferation rate in five MPV17-silenced cancer cell lines with two different shRNAs. How- ever, shRNA-mediated MPV17 knockdown performed in this work provided misguiding results regarding the resulting proliferation phenotype and only a rescue experiment was able to shed definitive light on the implication of MPV17 in cancer cell proliferation. Our results therefore emphasize the caution that is required when scientific conclusions are drawn from a work based on lentiviral vector-based gene silencing and clearly demonstrate the need to systematically perform a rescue experiment in order to ascertain the specific nature of the experimental results.

Published
2020

12. MPV17 does not control cancer cell proliferation

Author

Canonne, Morgane, primary, Wanet, Anaïs, additional, Nguyen, Thuy Truong An, additional, Khelfi, Alexis, additional, Ayama-Canden, Sophie, additional, Van Steenbrugge, Martine, additional, Fattaccioli, Antoine, additional, Sokal, Etienne, additional, Najimi, Mustapha, additional, Arnould, Thierry, additional, and Renard, Patricia, additional

Published
2020
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16. Effects of a sublethal and transient stress of the endoplasmic reticulum on the mitochondrial population

Author

Vannuvel, Kayleen, Van Steenbrugge, Martine, Demazy, Catherine, Ninane, Noëlle, Fattaccioli, Antoine, Fransolet, Maude, Renard, Patricia, Raes, Martine, and Arnould, Thierry

Abstract

Endoplasmic reticulum (ER) and mitochondria are not discrete intracellular organelles but establish close physical and functional interactions involved in several biological processes including mitochondrial bioenergetics, calcium homeostasis, lipid synthesis and the regulation of apoptotic cell death pathways. As many cell types might face a transient and sublethal ER stress during their lifetime, it is thus likely that the adaptive UPR response might affect the mitochondrial population. The aim of this work was to study the putative effects of a non-lethal and transient endoplasmic reticulum stress on the mitochondrial population in HepG2 cells. The results show that thapsigargin and brefeldin A, used to induce a transient and sublethal ER stress, rapidly lead to the fragmentationof the mitochondrial network associated with a decrease in mitochondrial membrane potential, O2.- production and less efficient respiration. These changes in mitochondrial function are transient and preceeded by the phosphorylation of JNK. Inhibition of JNK activation by SP600125 prevents thedecrease in O2.- production and the mitochondrial network fragmentation observed in cells exposed to the ER stress but has no impact on the reduction of the mitochondrial membrane potential. In conclusion, our data shows that a non-lethal and transient ER stress triggers a rapid activation of JNK without inducing apoptosis, leading to the fragmentation of the mitochondrial network and areduction of O2.- production.

Published
2016

17. The Transcription Factor 7-Like 2–Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1 Alpha Axis Connects Mitochondrial Biogenesis and Metabolic Shift with Stem Cell Commitment to Hepatic Differentiation

Author

Wanet, Anaïs, primary, Caruso, Marino, additional, Domelevo Entfellner, Jean-Baka, additional, Najar, Mehdi, additional, Fattaccioli, Antoine, additional, Demazy, Catherine, additional, Evraerts, Jonathan, additional, El-Kehdy, Hoda, additional, Pourcher, Guillaume, additional, Sokal, Etienne, additional, Arnould, Thierry, additional, Tiffin, Nicki, additional, Najimi, Mustapha, additional, and Renard, Patricia, additional

Published
2017
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20. Hybrid Alginate@TiO2Porous Microcapsules as a Reservoir of Animal Cells for Cell Therapy

Author

Leroux, Grégory, Neumann, Myriam, Meunier, Christophe F., Fattaccioli, Antoine, Michiels, Carine, Arnould, Thierry, Wang, Li, and Su, Bao-Lian

Abstract

The number of patients suffering from diseases linked with hormone deficiency (e.g., type 1 diabetes mellitus) has significantly increased in recent years. As organ transplantation presents its limits, the design of novel robust devices for cell encapsulation is of great interest. The current study reports the design of a novel hybrid alginate microcapsule reinforced by titania via a biocompatible synthesis from an aqueous stable titania precursor (TiBALDH) and a cationic polyamine (PDDAC) under mild conditions. The biocompatibility of this one-pot synthesis was confirmed by evaluation of the cytotoxicity of the precursor, additive, product, and by-product. The morphology, structure, and properties of the obtained hybrid microcapsule were characterized in detail. The microcapsule displayed mesoporous, which was a key parameter to allow the diffusion of nutrients and metabolites and to avoid the entry of immune defenders. The hybrid microcapsule also showed enhanced mechanical stability compared to the pure alginate microcapsule, making it an ideal candidate as a cell reservoir. HepG2 model cells encapsulated in the hybrid microcapsules remained intact for 43 days as highlighted by fluorescent viability probes, their oxygen consumption, and their albumin secretion. The study provides a significant progress in the conception of the robust and biocompatible reservoirs of animal cells for cell therapy.

Published
2018
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22. Taxol-induced unfolded protein response activation in breast cancer cells exposed to hypoxia: ATF4 activation regulates autophagy and inhibits apoptosis

Author

Notte, Annick, primary, Rebucci, Magali, additional, Fransolet, Maude, additional, Roegiers, Edith, additional, Genin, Marie, additional, Tellier, Celine, additional, Watillon, Kassandra, additional, Fattaccioli, Antoine, additional, Arnould, Thierry, additional, and Michiels, Carine, additional

Published
2015
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24. Hybrid Alginate@TiO 2 Porous Microcapsules as a Reservoir of Animal Cells for Cell Therapy.

Author

Leroux G, Neumann M, Meunier CF, Fattaccioli A, Michiels C, Arnould T, Wang L, and Su BL

Subjects
Alginates chemistry, Capsules chemistry, Cations administration & dosage, Cations chemistry, Cell Survival drug effects, Hep G2 Cells, Humans, Oxygen Consumption drug effects, Polyamines chemistry, Titanium administration & dosage, Titanium chemistry, Alginates pharmacology, Capsules pharmacology, Cell- and Tissue-Based Therapy, Polyamines administration & dosage
Abstract

The number of patients suffering from diseases linked with hormone deficiency (e.g., type 1 diabetes mellitus) has significantly increased in recent years. As organ transplantation presents its limits, the design of novel robust devices for cell encapsulation is of great interest. The current study reports the design of a novel hybrid alginate microcapsule reinforced by titania via a biocompatible synthesis from an aqueous stable titania precursor (TiBALDH) and a cationic polyamine (PDDAC) under mild conditions. The biocompatibility of this one-pot synthesis was confirmed by evaluation of the cytotoxicity of the precursor, additive, product, and by-product. The morphology, structure, and properties of the obtained hybrid microcapsule were characterized in detail. The microcapsule displayed mesoporous, which was a key parameter to allow the diffusion of nutrients and metabolites and to avoid the entry of immune defenders. The hybrid microcapsule also showed enhanced mechanical stability compared to the pure alginate microcapsule, making it an ideal candidate as a cell reservoir. HepG2 model cells encapsulated in the hybrid microcapsules remained intact for 43 days as highlighted by fluorescent viability probes, their oxygen consumption, and their albumin secretion. The study provides a significant progress in the conception of the robust and biocompatible reservoirs of animal cells for cell therapy.

Published
2018
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25. Hypersensitivity of mtDNA-depleted cells to staurosporine-induced apoptosis: roles of Bcl-2 downregulation and cathepsin B.

Author

Rommelaere G, Michel S, Mercy L, Fattaccioli A, Demazy C, Ninane N, Houbion A, Renard P, and Arnould T

Subjects
Caspase 3 metabolism, Cathepsin B antagonists & inhibitors, Cell Line, Tumor, Cytochromes c metabolism, DNA Fragmentation, Dipeptides pharmacology, Humans, Myeloid Cell Leukemia Sequence 1 Protein, Poly (ADP-Ribose) Polymerase-1, Poly(ADP-ribose) Polymerases metabolism, Proto-Oncogene Proteins c-bcl-2 genetics, bcl-X Protein metabolism, Apoptosis genetics, Cathepsin B metabolism, DNA, Mitochondrial genetics, Down-Regulation, Enzyme Inhibitors pharmacology, Proto-Oncogene Proteins c-bcl-2 metabolism, Staurosporine pharmacology
Abstract

We show that mitochondrial DNA (mtDNA)-depleted 143B cells are hypersensitive to staurosporine-induced cell death as evidenced by a more pronounced DNA fragmentation, a stronger activation of caspase-3, an enhanced poly(ADP-ribose) polymerase-1 (PARP-1) cleavage, and a more dramatic cytosolic release of cytochrome c. We also show that B-cell CLL/lymphoma-2 (Bcl-2), B-cell lymphoma extra large (Bcl-X(L)), and myeloid cell leukemia-1 (Mcl-1) are constitutively less abundant in mtDNA-depleted cells, that the inhibition of Bcl-2 and Bcl-X(L) can sensitize the parental cell line to staurosporine-induced apoptosis, and that overexpression of Bcl-2 or Bcl-X(L) can prevent the activation of caspase-3 in ρ(0)143B cells treated with staurosporine. Moreover, the inactivation of cathepsin B with CA074-Me significantly reduced cytochrome c release, caspase-3 activation, PARP-1 cleavage, and DNA fragmentation in mtDNA-depleted cells, whereas the pan-caspase inhibitor failed to completely prevent PARP-1 cleavage and DNA fragmentation in these cells, suggesting that caspase-independent mechanisms are responsible for cell death even if caspases are activated. Finally, we show that cathepsin B is released in the cytosol of ρ(0) cells in response to staurosporine, suggesting that the absence of mitochondrial activity leads to a facilitated permeabilization of lysosomal membranes in response to staurosporine.

Published
2011
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