Search

Your search keyword '"Zasso, Jacopo"' showing total 25 results
Start Over Author "Zasso, Jacopo"
25 results on '"Zasso, Jacopo"'

2. EGCG Disrupts the LIN28B/Let-7 Interaction and Reduces Neuroblastoma Aggressiveness.

Author

Cocchi, Simona, Greco, Valentina, Sidarovich, Viktoryia, Vigna, Jacopo, Broso, Francesca, Corallo, Diana, Zasso, Jacopo, Re, Angela, Rosatti, Emanuele Filiberto, Longhi, Sara, Defant, Andrea, Ladu, Federico, Sanna, Vanna, Adami, Valentina, D'Agostino, Vito G., Sturlese, Mattia, Sechi, Mario, Aveic, Sanja, Mancini, Ines, and Sighel, Denise

Subjects
NEUROBLASTOMA, TUMORS in children, CHILDHOOD cancer, RNA-binding proteins, PEDIATRIC oncology, CHILD death
Abstract

Neuroblastoma (NB) is the most commonly diagnosed extracranial solid tumor in children, accounting for 15% of all childhood cancer deaths. Although the 5-year survival rate of patients with a high-risk disease has increased in recent decades, NB remains a challenge in pediatric oncology, and the identification of novel potential therapeutic targets and agents is an urgent clinical need. The RNA-binding protein LIN28B has been identified as an oncogene in NB and is associated with a poor prognosis. Given that LIN28B acts by negatively regulating the biogenesis of the tumor suppressor let-7 miRNAs, we reasoned that selective interference with the LIN28B/let-7 miRNA interaction would increase let-7 miRNA levels, ultimately leading to reduced NB aggressiveness. Here, we selected (−)-epigallocatechin 3-gallate (EGCG) out of 4959 molecules screened as the molecule with the best inhibitory activity on LIN28B/let-7 miRNA interaction and showed that treatment with PLC/PLGA-PEG nanoparticles containing EGCG (EGCG-NPs) led to an increase in mature let-7 miRNAs and a consequent inhibition of NB cell growth. In addition, EGCG-NP pretreatment reduced the tumorigenic potential of NB cells in vivo. These experiments suggest that the LIN28B/let-7 miRNA axis is a good therapeutic target in NB and that EGCG, which can interfere with this interaction, deserves further preclinical evaluation. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

3. CAG repeat expansion in the Huntington’s disease gene shapes linear and circular RNAs biogenesis

Author

Ayyildiz, Dilara, primary, Bergonzoni, Guendalina, additional, Monziani, Alan, additional, Tripathi, Takshashila, additional, Döring, Jessica, additional, Kerschbamer, Emanuela, additional, Di Leva, Francesca, additional, Pennati, Elia, additional, Donini, Luisa, additional, Kovalenko, Marina, additional, Zasso, Jacopo, additional, Conti, Luciano, additional, Wheeler, Vanessa C., additional, Dieterich, Christoph, additional, Piazza, Silvano, additional, Dassi, Erik, additional, and Biagioli, Marta, additional

Published
2023
Full Text
View/download PDF

5. D12 Faulty linear and back-splicing in Huntington’s disease: novel players in the pathologic process hint at innovative RNA biomarkers

Author

Pellegrini, Miguel, primary, Ayyildiz, Dilara, additional, Bergonzoni, Guendalina, additional, Monziani, Alan, additional, Tripathi, Takshashila, additional, Döring, Jessica, additional, Cardamone, Giulia, additional, Kerschbamer, Emanuela, additional, Di Leva, Francesca, additional, Perrone, F, additional, Abruzzese, MP, additional, Busi, LC, additional, Asselta, Rosanna, additional, Pennati, Elia, additional, Donini, Luisa, additional, Zasso, Jacopo, additional, Conti, Luciano, additional, Wheeler, Vanessa C, additional, Dieterich, Christoph, additional, Piazza, Silvano, additional, Dassi, Erik, additional, Squitieri, Ferdinando, additional, and Biagioli, Marta, additional

Published
2022
Full Text
View/download PDF

6. Defective linear and circular RNAs biogenesis in Huntington’s disease: CAG repeat expansion hijacks neuronal splicing

Author

Ayyildiz, Dilara, primary, Monziani, Alan, additional, Tripathi, Takshashila, additional, Döring, Jessica, additional, Bergonzoni, Guendalina, additional, Kerschbamer, Emanuela, additional, Di Leva, Francesca, additional, Pennati, Elia, additional, Donini, Luisa, additional, Kovalenko, Marina, additional, Zasso, Jacopo, additional, Conti, Luciano, additional, Wheeler, Vanessa C., additional, Dieterich, Christoph, additional, Piazza, Silvano, additional, Dassi, Erik, additional, and Biagioli, Marta, additional

Published
2021
Full Text
View/download PDF

9. One-shot analysis of translated mammalian lncRNAs with AHARIBO

Author

Minati, Luca, primary, Firrito, Claudia, additional, Del Piano, Alessia, additional, Peretti, Alberto, additional, Sidoli, Simone, additional, Peroni, Daniele, additional, Belli, Romina, additional, Gandolfi, Francesco, additional, Romanel, Alessandro, additional, Bernabo, Paola, additional, Zasso, Jacopo, additional, Quattrone, Alessandro, additional, Guella, Graziano, additional, Lauria, Fabio, additional, Viero, Gabriella, additional, and Clamer, Massimiliano, additional

Published
2021
Full Text
View/download PDF

10. Author response: One-shot analysis of translated mammalian lncRNAs with AHARIBO

Author

Minati, Luca, primary, Firrito, Claudia, additional, Del Piano, Alessia, additional, Peretti, Alberto, additional, Sidoli, Simone, additional, Peroni, Daniele, additional, Belli, Romina, additional, Gandolfi, Francesco, additional, Romanel, Alessandro, additional, Bernabo, Paola, additional, Zasso, Jacopo, additional, Quattrone, Alessandro, additional, Guella, Graziano, additional, Lauria, Fabio, additional, Viero, Gabriella, additional, and Clamer, Massimiliano, additional

Published
2020
Full Text
View/download PDF

11. Artificial cells drive neural differentiation

Author

Toparlak, Ö. Duhan, primary, Zasso, Jacopo, additional, Bridi, Simone, additional, Serra, Mauro Dalla, additional, Macchi, Paolo, additional, Conti, Luciano, additional, Baudet, Marie-Laure, additional, and Mansy, Sheref S., additional

Published
2020
Full Text
View/download PDF

12. One-shot analysis of translated mammalian lncRNAs with AHARIBO

Author

Minati, Luca, primary, Firrito, Claudia, additional, Piano, Alessia Del, additional, Peretti, Alberto, additional, Sidoli, Simone, additional, Peroni, Daniele, additional, Belli, Romina, additional, Gandolfi, Francesco, additional, Romanel, Alessandro, additional, Bernabò, Paola, additional, Zasso, Jacopo, additional, Quattrone, Alessandro, additional, Guella, Graziano, additional, Lauria, Fabio, additional, Viero, Gabriella, additional, and Clamer, Massimiliano, additional

Published
2020
Full Text
View/download PDF

13. Vertically-Aligned Functionalized Silicon Micropillars for 3D Culture of Human Pluripotent Stem Cell-Derived Cortical Progenitors

Author

Cutarelli, Alessandro, primary, Ghio, Simone, additional, Zasso, Jacopo, additional, Speccher, Alessandra, additional, Scarduelli, Giorgina, additional, Roccuzzo, Michela, additional, Crivellari, Michele, additional, Maria Pugno, Nicola, additional, Casarosa, Simona, additional, Boscardin, Maurizio, additional, and Conti, Luciano, additional

Published
2019
Full Text
View/download PDF

14. Identification of REST-Regulated Molecular Circuitries and Targets Exploitable for hGSCs-Targeted Therapies

Author

Zasso, Jacopo and Conti, Luciano

Subjects
BIO/13 BIOLOGIA APPLICATA
Abstract

Glioblastoma (GBM) represents the most frequent and lethal cancer affecting the central nervous system for which no cure is currently available. The presence of Glioma Stem Cells (GSCs) has been proposed to be at the root of therapeutic failures due to their intrinsic abilities of escaping common treatments and relapsing the pathology. Thus, advances in therapeutic options may derive from the manipulation of mechanisms controlling the GSCs self-renewal, survival and functions. RE1-Silencing Transcription Factor (REST) is a master repressor of neuronal developmental programme in non-neuronal lineages, recently described as a main actor in the maintenance of the GSCs’ tumorigenic competence as its knockdown strongly impairs GSCs stemness both in vitro and in vivo. However, REST is critical for restraining neuronal cellular identity in various tissues, so that a targeted therapy to this transcriptional repressor is likely to present numerous side effects. Here, by taking advantage of a Tet-on system for the manipulation of REST expression in both human GSCs and Neural Stem Cell lines (hNSCs), we performed a transcriptomic profiling analysis in order to identify novel tumour-specific REST-regulated functions and molecular targets. Our analyses confirmed the previously reported roles of REST in neural tissues and enlightened novel REST functions in hGSCs, including the regulation of alternative hGSCs identity/state. Finally, analysis of hGSC-specific REST-regulated genes in GBM patients’ dataset revealed an inverse correlation with glioma aggressiveness, thus establishing a hGSC REST score that might provide a useful prognostic tool.

Published
2018

16. Identification of REST-Regulated Molecular Circuitries and Targets Exploitable for hGSCs-Targeted Therapies

Author

Conti, Luciano, Zasso, Jacopo, Conti, Luciano, and Zasso, Jacopo

Abstract

Glioblastoma (GBM) represents the most frequent and lethal cancer affecting the central nervous system for which no cure is currently available. The presence of Glioma Stem Cells (GSCs) has been proposed to be at the root of therapeutic failures due to their intrinsic abilities of escaping common treatments and relapsing the pathology. Thus, advances in therapeutic options may derive from the manipulation of mechanisms controlling the GSCs self-renewal, survival and functions. RE1-Silencing Transcription Factor (REST) is a master repressor of neuronal developmental programme in non-neuronal lineages, recently described as a main actor in the maintenance of the GSCs’ tumorigenic competence as its knockdown strongly impairs GSCs stemness both in vitro and in vivo. However, REST is critical for restraining neuronal cellular identity in various tissues, so that a targeted therapy to this transcriptional repressor is likely to present numerous side effects. Here, by taking advantage of a Tet-on system for the manipulation of REST expression in both human GSCs and Neural Stem Cell lines (hNSCs), we performed a transcriptomic profiling analysis in order to identify novel tumour-specific REST-regulated functions and molecular targets. Our analyses confirmed the previously reported roles of REST in neural tissues and enlightened novel REST functions in hGSCs, including the regulation of alternative hGSCs identity/state. Finally, analysis of hGSC-specific REST-regulated genes in GBM patients’ dataset revealed an inverse correlation with glioma aggressiveness, thus establishing a hGSC REST score that might provide a useful prognostic tool.

Published
2018

17. Vertically-Aligned Functionalized Silicon Micropillars for 3D Culture of Human Pluripotent Stem Cell-Derived Cortical Progenitors.

Author

Cutarelli, Alessandro, Ghio, Simone, Zasso, Jacopo, Speccher, Alessandra, Scarduelli, Giorgina, Roccuzzo, Michela, Crivellari, Michele, Pugno, Nicola Maria, Casarosa, Simona, Boscardin, Maurizio, and Conti, Luciano

Subjects
CEREBRAL cortex, SILICON, HUMAN embryology, TISSUE engineering, MORPHOLOGY, NEUROGLIA
Abstract

Silicon is a promising material for tissue engineering since it allows to produce micropatterned scaffolding structures resembling biological tissues. Using specific fabrication methods, it is possible to build aligned 3D network-like structures. In the present study, we exploited vertically-aligned silicon micropillar arrays as culture systems for human iPSC-derived cortical progenitors. In particular, our aim was to mimic the radially-oriented cortical radial glia fibres that during embryonic development play key roles in controlling the expansion, radial migration and differentiation of cortical progenitors, which are, in turn, pivotal to the establishment of the correct multilayered cerebral cortex structure. Here we show that silicon vertical micropillar arrays efficiently promote expansion and stemness preservation of human cortical progenitors when compared to standard monolayer growth conditions. Furthermore, the vertically-oriented micropillars allow the radial migration distinctive of cortical progenitors in vivo. These results indicate that vertical silicon micropillar arrays can offer an optimal system for human cortical progenitors’ growth and migration. Furthermore, similar structures present an attractive platform for cortical tissue engineering. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

25. Epsins regulate mouse embryonic stem cell exit from pluripotency and neural commitment by controlling notch activation

Author

Giuseppina Di Giacomo, Matteo Marcatili, Luca Ruggiero, Marina Cardano, Ottavio Cremona, Luciano Conti, Jacopo Zasso, Cardano, Marina, Zasso, Jacopo, Ruggiero, Luca, Di Giacomo, Giuseppina, Marcatili, Matteo, Cremona, Ottavio, and Conti, Luciano

Subjects
lcsh:Internal medicine, Histology, Epsin, Notch, Article Subject, media_common.quotation_subject, Notch signaling pathway, Biology, Endocytosis, endocytosis, Progenitor cell, lcsh:RC31-1245, Internalization, Molecular Biology, media_common, Gene knockdown, Cell Biology, pluripotency, Embryonic stem cell, Neural stem cell, Cell biology, Embryonic Stem cells, Epsin, endocytosis, Notch, pluripotency, Embryonic Stem cells, Research Article
Abstract

Epsins are part of the internalization machinery pivotal to control clathrin-mediated endocytosis. Here, we report that epsin family members are expressed in mouse embryonic stem cells (mESCs) and that epsin1/2 knockdown alters both mESC exits from pluripotency and their differentiation. Furthermore, we show that epsin1/2 knockdown compromises the correct polarization and division of mESC-derived neural progenitors and their conversion into expandable radial glia-like neural stem cells. Finally, we provide evidence that Notch signaling is impaired following epsin1/2 knockdown and that experimental restoration of Notch signaling rescues the epsin-mediated phenotypes. We conclude that epsins contribute to control mESC exit from pluripotency and allow their neural differentiation by appropriate modulation of Notch signaling.

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results