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1. ProNGF promotes brain metastasis through TrkA/EphA2 induced Src activation in triple negative breast cancer cells

Author

Cicero, Julien, Trouvilliez, Sarah, Palma, Martine, Ternier, Gaetan, Decoster, Laurine, Happernegg, Eloise, Barois, Nicolas, Van Outryve, Alexandre, Dehouck, Lucie, Bourette, Roland P., Adriaenssens, Eric, Lagadec, Chann, Tarhan, Cagatay Mehmet, Collard, Dominique, Souguir, Zied, Vandenhaute, Elodie, Maubon, Grégory, Sipieter, François, Borghi, Nicolas, Shimizu, Fumitaka, Kanda, Takashi, Giacobini, Paolo, Gosselet, Fabien, Maubon, Nathalie, Le Bourhis, Xuefen, Van Seuningen, Isabelle, Mysiorek, Caroline, and Toillon, Robert-Alain

Published
2023
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2. Direct interaction of TrkA/CD44v3 is essential for NGF-promoted aggressiveness of breast cancer cells

Author

Trouvilliez, Sarah, Cicero, Julien, Lévêque, Romain, Aubert, Léo, Corbet, Cyril, Van Outryve, Alexandre, Streule, Karolin, Angrand, Pierre-Olivier, Völkel, Pamela, Magnez, Romain, Brysbaert, Guillaume, Mysiorek, Caroline, Gosselet, Fabien, Bourette, Roland, Adriaenssens, Eric, Thuru, Xavier, Lagadec, Chann, de Ruyck, Jérôme, Orian-Rousseau, Véronique, Le Bourhis, Xuefen, and Toillon, Robert-Alain

Published
2022
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3. Spatial self-organization of cancer stem cell niches revealed by live single-cell imaging

Author

Brule, Mathilde, primary, Horochowska, Anais, additional, Fontaine, Emeline, additional, Torero-Ibad, Raoul, additional, Woesteland, Flavie, additional, Denoulet, Marie, additional, Pesez, Jean, additional, Adriaenssens, Eric, additional, Toillon, Robert-Alain, additional, Le-Bourhis, Xuefen, additional, Pfeuty, Benjamin, additional, Lagadec, Chann, additional, and Anquez, Francois, additional

Published
2024
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5. CXCL1/CXCR2 and CCL5/CCR1/CCR5 Promote Radiation-Induced Reprogramming of Breast Non-cancer Stem Cells into Cancer Stem Cells and Predict Patient Clinical Outcome

Author

Bailleul, Justine, primary, Brulé, Mathilde, additional, Bidan, Nadège, additional, Denoulet, Marie, additional, Mouttet Audouard, Raphaelle, additional, Cousin, Sophie, additional, Bouchaert, Emmanuel, additional, Benoit, Jerome, additional, Toillon, Robert-Alain, additional, Finetti, Pascal, additional, Birnbaum, Daniel, additional, Bertucci, François, additional, Adriaenssens, Eric, additional, Le Bourhis, Xuefen, additional, and Lagadec, Chann, additional

Published
2024
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7. Survival and self-renewing capacity of breast cancer initiating cells during fractionated radiation treatment

Author

Lagadec, Chann, Vlashi, Erina, Della Donna, Lorenza, Meng, YongHong, Dekmezian, Carmen, Kim, Kwanghee, and Pajonk, Frank

Abstract

Abstract Introduction Recent data indicate a hierarchical organization of many solid cancers, including breast cancer, with a small number of cancer initiating cells (CICs) that have the ability to self-renew and exhibit multi-lineage potency. We, and others, have demonstrated that CICs in breast cancer and glioma are relatively resistant to ionizing radiation if compared to their non-tumorigenic counterparts. However, the extent of the remaining self-renewing capacity of CICs after fractions of radiation is currently unknown. We hypothesized that CICs, in contrast to their non-tumorigenic counterparts, not only survive fractions of ionizing radiation but also retain the CIC phenotype as defined by operational means. Methods We used two marker systems to identify breast CICs (CD24-/low/CD44high, or lack of proteasome activity) and performed sphere-forming assays after multiple clinical fractions of radiation. Lineage tracking was performed by membrane staining. Cell cycle distribution and RNA content were assessed by flow cytometry and senescence was assessed via β-galactosidase staining. Results We demonstrated that irradiated CICs survived and retained their self-renewal capacity for at least four generations. We show that fractionated radiation not only spared CICs but also mobilized them from a quiescent/G0 phase of the cell cycle into actively cycling cells, while the surviving non-tumorigenic cells were driven into senescence. Conclusions The breast CIC population retains increased self-renewal capacity over several generations and therefore, we conclude that increases in the number of CICs after sublethal doses of radiation have potential clinical importance. Prevention of this process may lead to improved clinical outcome.

Published
2010

8. Data from Ionizing Radiation Activates the Nrf2 Antioxidant Response

Author

McDonald, J. Tyson, primary, Kim, Kwanghee, primary, Norris, Andrew J., primary, Vlashi, Erina, primary, Phillips, Tiffany M., primary, Lagadec, Chann, primary, Della Donna, Lorenza, primary, Ratikan, Josephine, primary, Szelag, Heather, primary, Hlatky, Lynn, primary, and McBride, William H., primary

Published
2023
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15. Single-cell Electrochemical Aptasensor Array

Author

Li, Shuo, primary, Coffinier, Yannick, additional, Lagadec, Chann, additional, Cleri, Fabrizio, additional, Nishiguchi, Katsuhiko, additional, Fujiwara, Akira, additional, Kim, Soo Hyeon, additional, and Clément, Nicolas, additional

Published
2023
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16. Silicon Compatible Process To Integrate Impedance Cytometry With Mechanical Characterization

Author

Rezard, Quentin, Shaik, Faruk Azam, Gerbedoen, Jean Claude, Cleri, Fabrizio, Collard, Dominique, Lagadec, Chann, Tarhan, Mehmet, Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL), Laboratory for Integrated Micro Mechatronics Systems (LIMMS), The University of Tokyo (UTokyo)-Centre National de la Recherche Scientifique (CNRS), University of Lille, Institut pour la recherche sur le cancer de Lille [Lille] (IRCL), Physique - IEMN (PHYSIQUE - IEMN), Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), and Bio-Micro-Electro-Mechanical Systems - IEMN (BIOMEMS - IEMN)

Subjects
microfabrication, impedance cytometry, single-cell analysis, [PHYS.PHYS.PHYS-INS-DET]Physics [physics]/Physics [physics]/Instrumentation and Detectors [physics.ins-det], [SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SPI.NANO]Engineering Sciences [physics]/Micro and nanotechnologies/Microelectronics, 3D electrodes
Abstract

International audience; This work is in the framework of SMMiL-E activities (a joint project of CNRS, Institute of Industrial Science,Centre Oscar Lambret, and the University of Lille). The authors acknowledge the French State-Region plan (CPER IRICL, Lille Interdisciplinary research Institute against cancer) for financial support and IRCL for hosting SMMiL-E. M.C. Tarhan and Q. Rezard acknowledge I-SITE ULNE.

Published
2023
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20. Metabolic state of glioma stem cells and nontumorigenic cells

Author

Vlashi, Erina, Lagadec, Chann, Vergnes, Laurent, Matsutani, Tomoo, Masui, Kenta, Poulou, Maria, Popescu, Ruxandra, Donna, Lorenza Della, Evers, Patrick, Dekmezian, Carmen, Reue, Karen, Christofk, Heather, Mischel, Paul S., and Pajonk, Frank

Published
2011

21. Direct interaction of TrkA/CD44v3 is essential for NGF-promoted aggressiveness of breast cancer cells

Author

UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, Trouvilliez, Sarah, Cicero, Julien, Lévêque, Romain, Aubert, Léo, Corbet, Cyril, Van Outryve, Alexandre, Streule, Karolin, Angrand, Pierre-Olivier, Völkel, Pamela, Magnez, Romain, Brysbaert, Guillaume, Mysiorek, Caroline, Gosselet, Fabien, Bourette, Roland, Adriaenssens, Eric, Thuru, Xavier, Lagadec, Chann, de Ruyck, Jérôme, Orian-Rousseau, Véronique, Le Bourhis, Xuefen, Toillon, Robert-Alain, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, Trouvilliez, Sarah, Cicero, Julien, Lévêque, Romain, Aubert, Léo, Corbet, Cyril, Van Outryve, Alexandre, Streule, Karolin, Angrand, Pierre-Olivier, Völkel, Pamela, Magnez, Romain, Brysbaert, Guillaume, Mysiorek, Caroline, Gosselet, Fabien, Bourette, Roland, Adriaenssens, Eric, Thuru, Xavier, Lagadec, Chann, de Ruyck, Jérôme, Orian-Rousseau, Véronique, Le Bourhis, Xuefen, and Toillon, Robert-Alain

Abstract

Background: CD44 is a multifunctional membrane glycoprotein. Through its heparan sulfate chain, CD44 presents growth factors to their receptors. We have shown that CD44 and Tropomyosin kinase A (TrkA) form a complex following nerve growth factor (NGF) induction. Our study aimed to understand how CD44 and TrkA interact and the consequences of inhibiting this interaction regarding the pro-tumoral effect of NGF in breast cancer. Methods: After determining which CD44 isoforms (variants) are involved in forming the TrkA/CD44 complex using proximity ligation assays, we investigated the molecular determinants of this interaction. By molecular modeling, we isolated the amino acids involved and confirmed their involvement using mutations. A CD44v3 mimetic peptide was then synthesized to block the TrkA/CD44v3 interaction. The effects of this peptide on the growth, migration and invasion of xenografted triple-negative breast cancer cells were assessed. Finally, we investigated the correlations between the expression of the TrkA/CD44v3 complex in tumors and histo-pronostic parameters. Results: We demonstrated that isoform v3 (CD44v3), but not v6, binds to TrkA in response to NGF stimulation. The final 10 amino acids of exon v3 and the TrkA H112 residue are necessary for the association of CD44v3 with TrkA. Functionally, the CD44v3 mimetic peptide impairs not only NGF-induced RhoA activation, clonogenicity, and migration/invasion of breast cancer cells in vitro but also tumor growth and metastasis in a xenograft mouse model. We also detected TrkA/CD44v3 only in cancerous cells, not in normal adjacent tissues.

Published
2022

23. Single cell classification using statistical learning on mechanical properties measured by mems tweezers

Author

Ahmadian, Bahram, Mbujamba, Deborah, Gerbedoen, Jean Claude, Kumemura, Momoko, Fujita, Hiroyuki, Collard, Dominique, Dabo-Niang, Sophie, Lagadec, Chann, Tarhan, Mehmet, Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL), Bio-Micro-Electro-Mechanical Systems - IEMN (BIOMEMS - IEMN), Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), JUNIA (JUNIA), Université catholique de Lille (UCL), Laboratory for Integrated Micro Mechatronics Systems (LIMMS), The University of Tokyo (UTokyo)-Centre National de la Recherche Scientifique (CNRS), Kyushu Institute of Technology (Kyutech), MOdel for Data Analysis and Learning (MODAL), Laboratoire Paul Painlevé (LPP), Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université de Lille, Sciences et Technologies-Inria Lille - Nord Europe, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Evaluation des technologies de santé et des pratiques médicales - ULR 2694 (METRICS), Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-École polytechnique universitaire de Lille (Polytech Lille), Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), This work is in the framework of SMMiL-E activities (a joint project of CNRS, Institute of Industrial Science, Centre Oscar Lambret and University of Lille) and supported by a grant from Contrat de Plan Etat-Region CPER Cancer 2015–2020, and Ruban Rose award. The authors acknowledge IRCL for hosting SMMiL-E. M. C. Tarhan acknowledge I-SITE ULNE., Laboratoire Paul Painlevé - UMR 8524 (LPP), Centre National de la Recherche Scientifique (CNRS)-Université de Lille, his work is in the framework of SMMiL-E activities (a joint project of CNRS, Institute of Industrial Science, Centre Oscar Lambret and University of Lille) and supported by a grant from Contrat de Plan Etat-Region CPER Cancer 2015–2020, and Ruban Rose award. The authors acknowledge IRCL for hosting SMMiL-E. M. C. Tarhan acknowledge I-SITE ULNE., and Dabo-Niang, Sophie

Subjects
[STAT]Statistics [stat], cancer cell classification, [SPI]Engineering Sciences [physics], Single-cell characterization, [SPI] Engineering Sciences [physics], MEMS tweezers, supervised learning, [STAT] Statistics [stat]
Abstract

International audience; Cell population is heterogenous and so presents a wide range of properties as metastatic potential. But using rare cells for clinical applications requires precise classification of individual cells. Here, we propose a multi-parameter analysis of single cells to classify them using statistical learning techniques and to predict the sub-population of each cell, although they may have close characteristics. We used MEMS tweezers to analyze mechanical properties (stiffness, viscosity, and size) of single cells from two different breast cancer cell lines in a controlled environment and run supervised learning methods to predict the population they belong to. This label-free method is a significant step forward to distinguish rare cell sub-populations for clinical applications.

Published
2022
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24. Additional file 3 of Direct interaction of TrkA/CD44v3 is essential for NGF-promoted aggressiveness of breast cancer cells

Author

Trouvilliez, Sarah, Cicero, Julien, Lévêque, Romain, Aubert, Léo, Corbet, Cyril, Van Outryve, Alexandre, Streule, Karolin, Angrand, Pierre-Olivier, Völkel, Pamela, Magnez, Romain, Brysbaert, Guillaume, Mysiorek, Caroline, Gosselet, Fabien, Bourette, Roland, Adriaenssens, Eric, Thuru, Xavier, Lagadec, Chann, de Ruyck, Jérôme, Orian-Rousseau, Véronique, Le Bourhis, Xuefen, and Toillon, Robert-Alain

Subjects
animal structures, nervous system
Abstract

Additional file 3: Supplementary Figure 1. Validation of the ectopic expression of CD44 and/or TrkA in COS-7 cells. The expression of all CD44 isoforms (A), CD44 variant 3 (B), CD44 variant 6 (C) and TrkA (hyaluronan [HA]; D) was evaluated by RT–qPCR (normalized using PUM-1). No expression of CD44, CD44 variants [3 or 6] or TrkA was detected in COS-7 cells (A-D) compared with that in cells transfected with the expression plasmid carrying each protein. Supplementary figure 2. TrkA does not interact with CD44s or CD44v6. Wild-type cos7 cells (A) or CD44S- (B) or CD44v6 (C) cells transfected with TrkA were treated with 100 ng/ml NGF (0, 5 or 30 min) and fixed. Quantification of the PLA results was performed using ImageJ software (30 randomly chosen fields per condition of three different experiments). Statistical analyses were performed using one-way ANOVA followed by Bonferroni’s posttest. The error bars represent the standard error of the mean (S.E.M.); ns, not significant. Supplementary Figure 3. CD44v3 and TrkA are recruited to the plasma membrane through NGF stimulation. CD44v3 and CD44v6 levels at the plasma membrane were assessed by flow cytometry (A-D). The plasma membrane and total TrkA and CD44v3 levels were also quantified by confocal microscopy (E-H). Statistical analyses were performed using one-way ANOVA followed by Bonferroni’s posttest. The error bars represent the standard error of the mean (S.E.M.); * p

Published
2022
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25. Neurotrophins promotes brain metastasis of triple negative breast cancer through Src kinase family activation

Author

Cicero, Julien, Trouvilliez, Sarah, Palma, Martine, Ternier, Gaetan, Decoster, Laurine, Barrois, Nicolas, Dehouck, Lucie, Happernegg, Eloise, Bourette, Roland, Adriaenssens, Eric, Lagadec, Chann, Tarhan, Mehmet, Collard, Dominique, Souguir, Zied, Vandenhaute, Elodie, Maubon, Grégory, Maubon, Nathalie, SIPIETER, FRANCOIS, Sipieter, François, Borghi, Nicolas, Giacobini, Paolo, Prevost, Vincent, Gosselet, Fabien, Le Bourhis, Xuefen, van Seuningen, Isabelle, Mysiorek, Caroline, Toillon, Robert-Alain, IEMN, Collection, Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de la Barrière Hémato-Encéphalique (LBHE), Université d'Artois (UA), Centre Régional de Lutte contre le Cancer Oscar Lambret [Lille] (UNICANCER/Lille), Université de Lille-UNICANCER, CHU Lille, Lille Neurosciences & Cognition - U 1172 (LilNCog), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Plateformes Lilloises en Biologie et Santé - UAR 2014 - US 41 (PLBS), Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL), Bio-Micro-Electro-Mechanical Systems - IEMN (BIOMEMS - IEMN), Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), JUNIA (JUNIA), Université catholique de Lille (UCL), Laboratory for Integrated Micro Mechatronics Systems (LIMMS), The University of Tokyo (UTokyo)-Centre National de la Recherche Scientifique (CNRS), HCS-Pharma Loos [Lille] (HCS-PL), Institut Jacques Monod (IJM (UMR_7592)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), and Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SPI]Engineering Sciences [physics], [SPI] Engineering Sciences [physics]
Abstract

ORAL; International audience; With nearly 2.3 million cases diagnosed worldwide each year and an estimated 685 000 deaths by 2020, breast cancer is the leading cause of cancer-related death in women. Brain metastases cause severe cognitive complications that severely impair quality of life. In TN breast cancer, the prognosis for brain metastases is particularly poor with a median survival of no more than 6 months. It is therefore crucial to know the molecular actors that promote the metastatic dissemination of triple negative breast cancer to the brain but also to prevent the proliferation of brain micrometastases that can cause fatal recurrences. In order to recapitulate several final stages of brain metastasis, we used both human Blood- Brain-Barrier in vitro model, human organotypic 3D extracellular in vitro matrix, mice brain slices organotypic ex vivo culture and in vivo mice xenograft. These models are coupled with single cell, 3D and real time imaging techniques, including FRET biosensing. This unique experimental approach allows us to study the involvement of signaling pathways in these different biological processes. Using this innovative method, we have identified that inhibition neurotrophins receptor leads to a decrease in the activity of the underlying signaling pathways and consequently to a decrease in the ability of breast cancer cells to pass through the BBB, to grow and to colonize the brain parenchyma.

Published
2022

34. Enhancement of Breast Cancer Cell Aggressiveness by lncRNA H19 and its Mir-675 Derivative: Insight into Shared and Different Actions

Author

Peperstraete, Evodie, Lecerf, Clément, Collette, Jordan, Vennin, Constance, Raby, Ludivine, Völkel, Pamela, Angrand, Pierre-Olivier, Winter, Marie, Bertucci, Francois, Finetti, Pascal, Lagadec, Chann, Meignan, Samuel, Bourette, Roland, Bourhis, Xuefen Le, Adriaenssens, Eric, Centre de Recherche en Cancérologie de Marseille (CRCM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Signalisation des Facteurs de Croissance Dans Le Cancer du Sein . Proteomique Fonctionnelle, Université de Lille, Sciences et Technologies-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM), Signalisation des facteurs de croissance dans le cancer du sein. Protéomique fonctionnelle, Institut de biologie de Lille - IBL (IBLI), Université de Lille, Sciences et Technologies-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS), Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Centre Régional de Lutte contre le Cancer Oscar Lambret [Lille] (UNICANCER/Lille), Université de Lille-UNICANCER, CHU Lille, Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Paoli-Calmettes, and Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)

Subjects
H19 gene, cancer stem cell, [SDV]Life Sciences [q-bio], [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, miR-675, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, female genital diseases and pregnancy complications, Article, LncRNA, breast cancer, tumoral progression, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], embryonic structures, ComputingMilieux_MISCELLANEOUS
Abstract

Breast cancer is a major public health problem and the leading world cause of women death by cancer. Both the recurrence and mortality of breast cancer are mainly caused by the formation of metastasis. The long non-coding RNA H19, the precursor of miR-675, is involved in breast cancer development. The aim of this work was to determine the implication but, also, the relative contribution of H19 and miR-675 to the enhancement of breast cancer metastatic potential. We showed that both H19 and miR-675 increase the invasive capacities of breast cancer cells in xenografted transgenic zebrafish models. In vitro, H19 and miR-675 enhance the cell migration and invasion, as well as colony formation. H19 seems to induce the epithelial-to-mesenchymal transition (EMT), with a decreased expression of epithelial markers and an increased expression of mesenchymal markers. Interestingly, miR-675 simultaneously increases the expression of both epithelial and mesenchymal markers, suggesting the induction of a hybrid phenotype or mesenchymal-to-epithelial transition (MET). Finally, we demonstrated for the first time that miR-675, like its precursor H19, increases the stemness properties of breast cancer cells. Altogether, our data suggest that H19 and miR-675 could enhance the aggressiveness of breast cancer cells through both common and different mechanisms.

Published
2020
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44. L'expression de s-SHIP identifie une population de cellules souches cancéreuses chez la souris

Author

Tian, Lu, Truong, Marie-José, Lagadec, Chann, Adriaenssens, Eric, Bouchaert, Emmanuel, Bauderlique-Le Roy, Hélène, Figeac, Martin, Le Bourhis, Xuefen, Bourette, Roland, Stanford School of Medicine [Stanford], Stanford Medicine, Stanford University-Stanford University, Signalisation des Facteurs de Croissance Dans Le Cancer du Sein . Proteomique Fonctionnelle, Université de Lille, Sciences et Technologies-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de biologie de Lille - IBL (IBLI), Université de Lille, Sciences et Technologies-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS), Site de Recherche Intégrée en Cancérologie (SIRIC-ONCOLille), Université de Lille, Sciences et Technologies-Université de Lille, Sciences Humaines et Sociales-Centre Régional de Lutte contre le Cancer Oscar Lambret [Lille] (UNICANCER/Lille), Université de Lille-UNICANCER-Université de Lille-UNICANCER-Cancéropole Nord-Ouest-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Plateforme de génomique fonctionnelle et structurelle [Lille], Institut pour la recherche sur le cancer de Lille [Lille] (IRCL)-Université de Lille, Droit et Santé, Signalisation des facteurs de croissance dans le cancer du sein. Protéomique fonctionnelle, Institut National de la Santé et de la Recherche Médicale (INSERM), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Centre National de la Recherche Scientifique (CNRS)-Université de Lille, Droit et Santé, and Université Lille Nord de France (COMUE)-UNICANCER-Université Lille Nord de France (COMUE)-UNICANCER-Cancéropole Nord-Ouest-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)

Subjects
[SDV.CAN]Life Sciences [q-bio]/Cancer, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2019
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45. A new pancreatic adenocarcinoma‐derived organoid model of acquired chemoresistance to FOLFIRINOX: First insight of the underlying mechanisms.

Author

Hadj Bachir, Elsa, Poiraud, Charles, Paget, Sonia, Stoup, Nicolas, El Moghrabi, Soumaya, Duchêne, Belinda, Jouy, Nathalie, Bongiovanni, Antonino, Tardivel, Meryem, Weiswald, Louis‐Bastien, Vandepeutte, Marie, Beugniez, César, Escande, Fabienne, Leteurtre, Emmanuelle, Poulain, Laurent, Lagadec, Chann, Pigny, Pascal, Jonckheere, Nicolas, Renaud, Florence, and Truant, Stephanie

Subjects
CANCER chemotherapy, DRUG resistance in cancer cells, PROGNOSIS, DRUG resistance, DRUG therapy, ANTIMETABOLITES
Abstract

Background Information: Although improvements have been made in the management of pancreatic adenocarcinoma (PDAC) during the past 20 years, the prognosis of this deadly disease remains poor with an overall 5‐year survival under 10%. Treatment with FOLFIRINOX, a combined regimen of 5‐fluorouracil, irinotecan (SN‐38) and oxaliplatin, is nonetheless associated with an excellent initial tumour response and its use has allowed numerous patients to go through surgery while their tumour was initially considered unresectable. These discrepancies between initial tumour response and very low long‐term survival are the consequences of rapidly acquired chemoresistance and represent a major therapeutic frontier. To our knowledge, a model of resistance to the combined three drugs has never been described due to the difficulty of modelling the FOLFIRINOX protocol both in vitro and in vivo. Patient‐derived tumour organoids (PDO) are the missing link that has long been lacking in the wide range of epithelial cancer models between 2D adherent cultures and in vivo xenografts. In this work we sought to set up a model of PDO with resistance to FOLFIRINOX regimen that we could compare to the paired naive PDO. Results: We first extrapolated physiological concentrations of the three drugs using previous pharmacodynamics studies and bi‐compartmental elimination models of oxaliplatin and SN‐38. We then treated PaTa‐1818x naive PDAC organoids with six cycles of 72 h‐FOLFIRINOX treatment followed by 96 h interruption. Thereafter, we systematically compared treated organoids to PaTa‐1818x naive organoids in terms of growth, proliferation, viability and expression of genes involved in cancer stemness and aggressiveness. Conclusions: We reproductively obtained resistant organoids FoxR that significantly showed less sensitivity to FOLFORINOX treatment than the PaTa‐1818x naive organoids from which they were derived. Our resistant model is representative of the sequential steps of chemoresistance observed in patients in terms of growth arrest (proliferation blockade), residual disease (cell quiescence/dormancy) and relapse. Significance: To our knowledge, this is the first genuine in vitro model of resistance to the three drugs in combined therapy. This new PDO model will be a great asset for the discovery of acquired chemoresistance mechanisms, knowledge that is mandatory before offering new therapeutic strategies for pancreatic cancer. [ABSTRACT FROM AUTHOR]

Published
2022
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47. AGENT-BASED GENETIC MULTICELLULAR 3D MODELLING OF STEM-CELL SPHEROIDS(GENESPHERE)

Author

Cleri, Fabrizio, Lagadec, Chann, Blossey, Ralf, Palla, Pier Luca, Giordano, Stefano, Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF), Physique - IEMN (PHYSIQUE - IEMN), Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF), Acoustique Impulsionnelle & Magnéto-Acoustique Non linéaire - Fluides, Interfaces Liquides & Micro-Systèmes - IEMN (AIMAN-FILMS - IEMN), Acoustique Impulsionnelle & Magnéto-Acoustique Non linéaire - Fluides, Interfaces Liquides & Micro-Systèmes - IEMN (AIMAN-FILMS-IEMN), Institut d’Électronique, de Microélectronique et de Nanotechnologie - Département Opto-Acousto-Électronique - UMR 8520 (IEMN-DOAE), Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-INSA Institut National des Sciences Appliquées Hauts-de-France (INSA Hauts-De-France)-Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), and Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-INSA Institut National des Sciences Appliquées Hauts-de-France (INSA Hauts-De-France)

Subjects
[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biophysics, [SDV]Life Sciences [q-bio], [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2018

48. Synuclein gamma expression enhances radiation resistance of breast cancer cells

Author

Tian, Lu, Zhao, Yucui, Truong, Marie-José, Lagadec, Chann, Bourette, Roland, Stanford School of Medicine [Stanford], Stanford Medicine, Stanford University-Stanford University, Signalisation des Facteurs de Croissance Dans Le Cancer du Sein . Proteomique Fonctionnelle, and Université de Lille, Sciences et Technologies-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV.CAN]Life Sciences [q-bio]/Cancer, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2018
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49. Transcriptomic Analysis of Breast Cancer Stem Cells and Development of a pALDH1A1:mNeptune Reporter System for Live Tracking

Author

Bidan, Nadège, primary, Bailleul‐Dubois, Justine, additional, Duval, Jérémy, additional, Winter, Marie, additional, Denoulet, Marie, additional, Hannebicque, Karine, additional, El‐Sayed, Ihsan Y., additional, Ginestier, Christophe, additional, Forissier, Violaine, additional, Charafe‐Jauffret, Emmanuelle, additional, Macario, Manon, additional, Matsunaga, Yukiko T, additional, Meignan, Samuel, additional, Anquez, François, additional, Julien, Sylvain, additional, Bonnefond, Amélie, additional, Derhourhi, Mehdi, additional, Le Bourhis, Xuefen, additional, and Lagadec, Chann, additional

Published
2019
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50. Nerve growth factor promotes breast cancer angiogenesis by activating multiple pathways

Author

Adriaenssens Eric, Romon Rodrigue, Lagadec Chann, Germain Emmanuelle, Hondermarck Hubert, and Le Bourhis Xuefen

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Although several anti-angiogenic therapies have been approved in the treatment of cancer, the survival benefits of such therapies are relatively modest. Discovering new molecules and/or better understating signaling pathways of angiogenesis is therefore essential for therapeutic improvements. The objective of the present study was to determine the involvement of nerve growth factor (NGF) in breast cancer angiogenesis and the underlying molecular mechanisms. Results We showed that both recombinant NGF and NGF produced by breast cancer cells stimulated angiogenesis in Matrigel plugs in immunodeficient mice. NGF strongly increased invasion, cord formation and the monolayer permeability of endothelial cells. Moreover, NGF-stimulated invasion was under the control of its tyrosine kinase receptor (TrkA) and downstream signaling pathways such as PI3K and ERK, leading to the activation of matrix metalloprotease 2 and nitric oxide synthase. Interestingly, NGF increased the secretion of VEGF in both endothelial and breast cancer cells. Inhibition of VEGF, with a neutralizing antibody, reduced about half of NGF-induced endothelial cell invasion and angiogenesis in vivo. Conclusions Our findings provided direct evidence that NGF could be an important stimulator for breast cancer angiogenesis. Thus, NGF, as well as the activated signaling pathways, should be regarded as potential new targets for anti-angiogenic therapy against breast cancer.

Published
2010
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