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29 results on '"Fransolet, Maude"'

3. 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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9. 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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11. Mitochondrial Protein Cox7b Is a Metabolic Sensor Driving Brain-Specific Metastasis of Human Breast Cancer Cells

Author

Blackman, Marine C. N. M., primary, Capeloa, Tania, additional, Rondeau, Justin D., additional, Zampieri, Luca X., additional, Benyahia, Zohra, additional, Van de Velde, Justine A., additional, Fransolet, Maude, additional, Daskalopoulos, Evangelos P., additional, Michiels, Carine, additional, Beauloye, Christophe, additional, and Sonveaux, Pierre, additional

Published
2022
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12. Mitochondrial Protein Cox7b Is a Metabolic Sensor Driving Brain-Specific Metastasis of Human Breast Cancer Cells

Author

UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UNamur - SBIO_URBC (unité de recherche en biologie cellulaire), Blackman, Marine, De Miranda Capeloa, Tania Isabel, Rondeau, Justin, Zampieri, Luca, Benyahia, Zohra, Van de Velde, Justine, Fransolet, Maude, Daskalopoulos, Evangelos P., Michiels, Carine, Beauloye, Christophe, Sonveaux, Pierre, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UNamur - SBIO_URBC (unité de recherche en biologie cellulaire), Blackman, Marine, De Miranda Capeloa, Tania Isabel, Rondeau, Justin, Zampieri, Luca, Benyahia, Zohra, Van de Velde, Justine, Fransolet, Maude, Daskalopoulos, Evangelos P., Michiels, Carine, Beauloye, Christophe, and Sonveaux, Pierre

Published
2022

13. MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

Author

Capeloa, Tania, Krzystyniak, Joanna, D'Hose, Donatienne, Canas Rodriguez, Amanda, Payen, Valery L, Zampieri, Luca X, Van De Velde, Justine A, Benyahia, Zohra, Pranzini, Erica, Vazeille, Thibaut, Fransolet, Maude, Bouzin, Caroline, Brusa, Davide, Michiels, Carine, Gallez, Bernard, Murphy, Mike, Porporato, Paolo E, Sonveaux, Pierre, Capeloa, Tania [0000-0001-8034-5524], d'Hose, Donatienne [0000-0002-5566-5259], Zampieri, Luca X [0000-0002-9286-7693], Van de Velde, Justine A [0000-0003-0054-9020], Pranzini, Erica [0000-0002-1668-2777], Bouzin, Caroline [0000-0003-0694-1947], Brusa, Davide [0000-0002-6499-9648], Michiels, Carine [0000-0002-9169-1294], Gallez, Bernard [0000-0002-5708-1302], Murphy, Mike [0000-0003-1115-9618], Porporato, Paolo E [0000-0001-8519-1552], Sonveaux, Pierre [0000-0001-6484-8834], Apollo - University of Cambridge Repository, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UCL - SSS/LDRI - Louvain Drug Research Institute, UNamur - SBIO_URBC (unité de recherche en biologie cellulaire), and Murphy, Michael P [0000-0003-1115-9618]

Subjects
Mitochondria-targeted antioxidant, Cancer Research, breast cancer, migration, invasion, clonogenicity, spheroids, metastasis, mitochondria, mitochondrial superoxide, MitoQ, mitochondria-targeted antioxidant, Metastasis, Mitochondria, Breast cancer, Invasion, Oncology, Clonogenicity, Spheroids, Migration, Mitochondrial superoxide
Abstract

To successfully generate distant metastases, metastatic progenitor cells must simultaneously possess mesenchymal characteristics, resist to anoïkis, migrate and invade directionally, resist to redox and shear stresses in the systemic circulation, and possess stem cell characteristics. These cells primarily originate from metabolically hostile areas of the primary tumor, where oxygen and nutrient deprivation, together with metabolic waste accumulation, exert a strong selection pressure promoting evasion. Here, we followed the hypothesis according to which metastasis as a whole implies the existence of metabolic sensors. Among others, mitochondria are singled out as a major source of superoxide that supports the metastatic phenotype. Molecularly, stressed cancer cells increase mitochondrial superoxide production, which activates the transforming growth factor-β pathway through src directly within mitochondria, ultimately activating focal adhesion kinase Pyk2. The existence of mitochondria-targeted antioxidants constitutes an opportunity to interfere with the metastatic process. Here, using aggressive triple-negative and HER2-positive human breast cancer cell lines as models, we report that MitoQ inhibits all the metastatic traits that we tested in vitro. Compared to other mitochondria-targeted antioxidants, MitoQ already successfully passed Phase I safety clinical trials, which provides an important incentive for future preclinical and clinical evaluations of this drug for the prevention of breast cancer metastasis.

Published
2022
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14. MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

Author

Capeloa, Tania, primary, Krzystyniak, Joanna, additional, d’Hose, Donatienne, additional, Canas Rodriguez, Amanda, additional, Payen, Valery L., additional, Zampieri, Luca X., additional, Van de Velde, Justine A., additional, Benyahia, Zohra, additional, Pranzini, Erica, additional, Vazeille, Thibaut, additional, Fransolet, Maude, additional, Bouzin, Caroline, additional, Brusa, Davide, additional, Michiels, Carine, additional, Gallez, Bernard, additional, Murphy, Michael P., additional, Porporato, Paolo E., additional, and Sonveaux, Pierre, additional

Published
2022
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19. 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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21. Characterization of the role of TMEM45A in cancer cell sensitivity to cisplatin.

Author

UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service d'oncologie médicale, Schmit, Kathleen, Chen, Jia-Wei, Ayama-Canden, Sophie, Fransolet, Maude, Finet, Laure, Demazy, Catherine, D'Hondt, Lionel, Graux, Carlos, Michiels, Carine, UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service d'oncologie médicale, Schmit, Kathleen, Chen, Jia-Wei, Ayama-Canden, Sophie, Fransolet, Maude, Finet, Laure, Demazy, Catherine, D'Hondt, Lionel, Graux, Carlos, and Michiels, Carine

Abstract

TMEM45A is a transmembrane protein involved in tumor progression and cancer resistance to chemotherapeutic agents in hypoxic condition. It is correlated to a low breast cancer patient overall survival. However, little is known about this protein, in particular the mechanisms by which TMEM45A modulates cancer cell chemosensitivity. In this work, the messenger RNA expression of TMEM45A was assessed in head and neck squamous cell carcinoma (HNSCC) and renal cell carcinoma (RCC) biopsies. TMEM45A was upregulated in patients diagnosed for head and neck or renal cancer. Then, the implication of this protein in cisplatin sensitivity was explored in SQD9 and RCC4 + pVHL cells. TMEM45A inactivation decreased cell proliferation and modulated cell responses to cisplatin. Indeed, TMEM45A inactivation increased the sensitivity of SQD9 cells to cisplatin, whereas it rendered RCC4 + pVHL cells resistant to this anticancer agent. Through RNA-sequencing analysis, we identified several deregulated pathways that indicated that the impact on cisplatin sensitivity may be associated to the inhibition of DNA damage repair and to UPR pathway activation. This study demonstrated, for the first time, an anti or a pro-apoptotic role of this protein depending on the cancer type and highlighted the role of TMEM45A in modulating patient responses to treatment.

Published
2019

23. 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
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29. Copper(ii) oxide nanoparticles penetrate into HepG2 cells, exert cytotoxicity via oxidative stress and induce pro-inflammatory response

Author

Piret, Jean-Pascal, primary, Jacques, Diane, additional, Audinot, Jean-Nicolas, additional, Mejia, Jorge, additional, Boilan, Emmanuelle, additional, Noël, Florence, additional, Fransolet, Maude, additional, Demazy, Catherine, additional, Lucas, Stéphane, additional, Saout, Christelle, additional, and Toussaint, Olivier, additional

Published
2012
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