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27 results on '"Ilari, Ramona"'

1. Extracellular vesicles produced by irradiated endothelial or Glioblastoma stem cells promote tumor growth and vascularization modulating tumor microenvironment

Author

Castellani, Giorgia, Buccarelli, Mariachiara, D’Alessandris, Quintino Giorgio, Ilari, Ramona, Cappannini, Andrea, Pedini, Francesca, Boe, Alessandra, Lulli, Valentina, Parolini, Isabella, Giannetti, Stefano, Biffoni, Mauro, Zappavigna, Vincenzo, Marziali, Giovanna, Pallini, Roberto, and Ricci-Vitiani, Lucia

Published
2024
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2. MiR-378a-3p Acts as a Tumor Suppressor in Colorectal Cancer Stem-Like Cells and Affects the Expression of MALAT1 and NEAT1 lncRNAs

Author

Castellani, Giorgia, primary, Buccarelli, Mariachiara, additional, Lulli, Valentina, additional, Ilari, Ramona, additional, De Luca, Gabriele, additional, Pedini, Francesca, additional, Boe, Alessandra, additional, Felli, Nadia, additional, Biffoni, Mauro, additional, Pilozzi, Emanuela, additional, Marziali, Giovanna, additional, and Ricci-Vitiani, Lucia, additional

Published
2022
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5. Deregulated expression of the imprinted DLK1-DIO3 region in Glioblastoma Stem-like Cells: tumor suppressor role of lncRNA MEG3

Author

Buccarelli, Mariachiara, Lulli, Valentina, Giuliani, Alessandro, Signore, Michele, Martini, Maurizio, D'Alessandris, Quintino Giorgio, Giannetti, Stefano, Novelli, Agnese, Ilari, Ramona, Giurato, Giorgio, Boe, Alessandra, Castellani, Giorgia, Spartano, Serena, Marangi, Giuseppe, Biffoni, Mauro, Genuardi, Maurizio, Pallini, Roberto, Marziali, Giovanna, Ricci-Vitiani, Lucia, Martini, Maurizio (ORCID:0000-0002-6260-6310), D'Alessandris, Quintino G (ORCID:0000-0002-2953-9291), Giannetti, Stefano (ORCID:0000-0002-9456-8865), Marangi, Giuseppe (ORCID:0000-0002-6898-8882), Genuardi, Maurizio (ORCID:0000-0002-7410-8351), Pallini, Roberto (ORCID:0000-0002-4611-8827), Buccarelli, Mariachiara, Lulli, Valentina, Giuliani, Alessandro, Signore, Michele, Martini, Maurizio, D'Alessandris, Quintino Giorgio, Giannetti, Stefano, Novelli, Agnese, Ilari, Ramona, Giurato, Giorgio, Boe, Alessandra, Castellani, Giorgia, Spartano, Serena, Marangi, Giuseppe, Biffoni, Mauro, Genuardi, Maurizio, Pallini, Roberto, Marziali, Giovanna, Ricci-Vitiani, Lucia, Martini, Maurizio (ORCID:0000-0002-6260-6310), D'Alessandris, Quintino G (ORCID:0000-0002-2953-9291), Giannetti, Stefano (ORCID:0000-0002-9456-8865), Marangi, Giuseppe (ORCID:0000-0002-6898-8882), Genuardi, Maurizio (ORCID:0000-0002-7410-8351), and Pallini, Roberto (ORCID:0000-0002-4611-8827)

Abstract

Background: Glioblastoma (GBM) stem-like cells (GSCs) are thought to be responsible for the maintenance and aggressiveness of GBM, the most common primary brain tumor in adults. This study aims at elucidating the involvement of deregulations within the imprinted DLK-DIO3 region on chromosome 14q32 in GBM pathogenesis. Methods: RT-PCR analyses were performed on GSCs and GBM tissues. Methylation analyses, gene expression and Reverse-Phase protein Array profiles were used to investigate the tumor suppressor function of MEG3. Results: Loss of expression of genes and non-coding RNAs within the DLK1-DIO3 region was observed in GSCs and GBM tissues compared to normal brain. This down-regulation is mainly mediated by epigenetic silencing. Kaplan-Meier analysis indicated that low expression of MEG3 and MEG8 lncRNAs significantly correlated with short survival in GBM patients. MEG3 restoration impairs tumorigenic abilities of GSCs in vitro by inhibiting cell growth, migration and colony formation and decreases in vivo tumor growth reducing infiltrative growth. These effects were associated with modulation of genes involved in cell adhesion and Epithelial to Mesenchymal Transition (EMT). Conclusions: In GBM, MEG3 acts as a tumor-suppressor mainly regulating cell adhesion, EMT and cell proliferation, thus providing a potential candidate for novel GBM therapies.

Published
2020

8. Deregulated expression of the imprinted DLK1-DIO3 region in glioblastoma stemlike cells: tumor suppressor role of lncRNA MEG3

Author

Buccarelli, Mariachiara, primary, Lulli, Valentina, additional, Giuliani, Alessandro, additional, Signore, Michele, additional, Martini, Maurizio, additional, D’Alessandris, Quintino G, additional, Giannetti, Stefano, additional, Novelli, Agnese, additional, Ilari, Ramona, additional, Giurato, Giorgio, additional, Boe, Alessandra, additional, Castellani, Giorgia, additional, Spartano, Serena, additional, Marangi, Giuseppe, additional, Biffoni, Mauro, additional, Genuardi, Maurizio, additional, Pallini, Roberto, additional, Marziali, Giovanna, additional, and Ricci-Vitiani, Lucia, additional

Published
2020
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9. Mir-370-3p Impairs Glioblastoma Stem-Like Cell Malignancy Regulating a Complex Interplay between HMGA2/HIF1A and the Oncogenic Long Non-Coding RNA (lncRNA) NEAT1

Author

Lulli, Valentina, primary, Buccarelli, Mariachiara, additional, Ilari, Ramona, additional, Castellani, Giorgia, additional, De Dominicis, Chiara, additional, Di Giamberardino, Alessandra, additional, D′Alessandris, Quintino Giorgio, additional, Giannetti, Stefano, additional, Martini, Maurizio, additional, Stumpo, Vittorio, additional, Boe, Alessandra, additional, De Luca, Gabriele, additional, Biffoni, Mauro, additional, Marziali, Giovanna, additional, Pallini, Roberto, additional, and Ricci-Vitiani, Lucia, additional

Published
2020
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16. miR-135b suppresses tumorigenesis in glioblastoma stem-like cells impairing proliferation, migration and self-renewal

Author

Lulli, Valentina, Buccarelli, Mariachiara, Martini, Maurizio, Signore, Michele, Biffoni, Mauro, Giannetti, Stefano, Morgante, Liliana, Marziali, Giovanna, Ilari, Ramona, Pagliuca, Alfredo, Larocca, Luigi Maria, De Maria Marchiano, Ruggero, Pallini, Roberto, Ricci-Vitiani, Lucia, Martini, Maurizio (ORCID:0000-0002-6260-6310), Giannetti, Stefano (ORCID:0000-0002-9456-8865), Larocca, Luigi Maria (ORCID:0000-0003-1739-4758), De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Pallini, Roberto (ORCID:0000-0002-4611-8827), Lulli, Valentina, Buccarelli, Mariachiara, Martini, Maurizio, Signore, Michele, Biffoni, Mauro, Giannetti, Stefano, Morgante, Liliana, Marziali, Giovanna, Ilari, Ramona, Pagliuca, Alfredo, Larocca, Luigi Maria, De Maria Marchiano, Ruggero, Pallini, Roberto, Ricci-Vitiani, Lucia, Martini, Maurizio (ORCID:0000-0002-6260-6310), Giannetti, Stefano (ORCID:0000-0002-9456-8865), Larocca, Luigi Maria (ORCID:0000-0003-1739-4758), De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), and Pallini, Roberto (ORCID:0000-0002-4611-8827)

Abstract

Glioblastoma multiforme (GBM) is the most common and fatal malignant adult primary brain tumor. Currently, the overall prognosis for GBM patients remains poor despite advances in neurosurgery and adjuvant treatments. MicroRNAs (miRNAs) contribute to the pathogenesis of various types of tumor, including GBM. In this study we analyzed the expression of a panel of miRNAs, which are known to be differentially expressed by the brain and GBM tumor, in a collection of patient-derived GBM stem-like cells (GSCs). Notably, the average expression level of miR-135b, was the most downregulated compared to its normal counterpart, suggesting a potential role as anti-oncogene. Restoration of miR-135b in GSCs significantly decreased proliferation, migration and clonogenic abilities. More importantly, miR-135b restoration was able to significantly reduce brain infiltration in mouse models of GBM obtained by intracerebral injection of GSC lines. We identified ADAM12 and confirmed SMAD5 and GSK3Î2 as miR-135b targets and potential mediators of its effects. The whole transcriptome analysis ascertained that the expression of miR-135b downmodulated additional genes driving key pathways in GBM survival and infiltration capabilities. Our results identify a critical role of miR-135b in the regulation of GBM development, suggesting that miR-135b might act as a tumor-suppressor factor and thus providing a potential candidate for the treatment of GBM patients.

Published
2015

17. miR-135b suppresses tumorigenesis in glioblastoma stem-like cells impairing proliferation, migration and self-renewal

Author

Lulli, Valentina, primary, Buccarelli, Mariachiara, additional, Martini, Maurizio, additional, Signore, Michele, additional, Biffoni, Mauro, additional, Giannetti, Stefano, additional, Morgante, Liliana, additional, Marziali, Giovanna, additional, Ilari, Ramona, additional, Pagliuca, Alfredo, additional, Larocca, Luigi Maria, additional, De Maria, Ruggero, additional, Pallini, Roberto, additional, and Ricci-Vitiani, Lucia, additional

Published
2015
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19. Critical Role of IRF-8 in Negative Regulation of TLR3 Expression by Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase-2 Activity in Human Myeloid Dendritic Cells

Author

Fragale, Alessandra, primary, Stellacci, Emilia, additional, Ilari, Ramona, additional, Remoli, Anna Lisa, additional, Lanciotti, Angela, additional, Perrotti, Edvige, additional, Shytaj, Iart, additional, Orsatti, Roberto, additional, Lawrence, Harshani R., additional, Lawrence, Nicholas J., additional, Wu, Jerry, additional, Rehli, Michael, additional, Ozato, Keiko, additional, and Battistini, Angela, additional

Published
2011
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21. IFN Regulatory Factor-1 Negatively Regulates CD4+CD25+ Regulatory T Cell Differentiation by Repressing Foxp3 Expression

Author

Fragale, Alessandra, primary, Gabriele, Lucia, additional, Stellacci, Emilia, additional, Borghi, Paola, additional, Perrotti, Edvige, additional, Ilari, Ramona, additional, Lanciotti, Angela, additional, Remoli, Anna Lisa, additional, Venditti, Massimo, additional, Belardelli, Filippo, additional, and Battistini, Angela, additional

Published
2008
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22. IRF-1 Is Required for Full NF-κB Transcriptional Activity at the Human Immunodeficiency Virus Type 1 Long Terminal Repeat Enhancer

Author

Sgarbanti, Marco, primary, Remoli, Anna L., additional, Marsili, Giulia, additional, Ridolfi, Barbara, additional, Borsetti, Alessandra, additional, Perrotti, Edvige, additional, Orsatti, Roberto, additional, Ilari, Ramona, additional, Sernicola, Leonardo, additional, Stellacci, Emilia, additional, Ensoli, Barbara, additional, and Battistini, Angela, additional

Published
2008
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23. Intracellular HIV-1 Tat protein represses constitutive LMP2 transcription increasing proteasome activity by interfering with the binding of IRF-1 to STAT1

Author

Remoli, Anna L., primary, Marsili, Giulia, additional, Perrotti, Edvige, additional, Gallerani, Eleonora, additional, Ilari, Ramona, additional, Nappi, Filomena, additional, Cafaro, Aurelio, additional, Ensoli, Barbara, additional, Gavioli, Riccardo, additional, and Battistini, Angela, additional

Published
2006
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25. Role of Ets-1 in transcriptional regulation of transferrin receptor and crythroid differentiation.

Author

Marziali, Giovanna, Perrotti, Edvige, Ilari, Ramona, Lulli, Valentina, Coccia, Eliana M., Moret, Remy, Kuhn, Lukas C., Testa, Ugo, and Battistini, Angela

Subjects
ERYTHROCYTE membranes, FRIEND virus, GENE expression
Abstract

Presents a study that characterized the minimal region able to confer transcriptional regulation during erythroid differentiation in Friend leukemia cells (FLC). Features of the region; Significance of Ets and Ap1/CRE like sites in the promoter activity during erythroid differentiation; Effect of the binding activity of Ets-1; Decrease in TfR gene expression in FLC.

Published
2002
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26. IRF-1 Is Required for Full NF-κ B Transcriptional Activity at the Human Immunodeficiency Virus Type 1 Long Terminal Repeat Enhancer.

Author

Sgarbanti, Marco, Remoli, Anna L., Marsili, Giulia, Ridolfi, Barbara, Borsetti, Alessandra, Perrotti, Edvige, Orsatti, Roberto, Ilari, Ramona, Sernicola, Leonardo, Stellacci, Emilia, Ensoli, Barbara, and Battistini, Angela

Subjects
*HIV, *GENE expression, *INTERFERONS, *RNA, *TRANSCRIPTION factors
Abstract

Human immunodeficiency virus type 1 (HIV-1) gene expression is controlled by a complex interplay between viral and host factors. We have previously shown that interferon-regulatory factor 1 (IRF-1) is stimulated early after HIV-1 infection and regulates promoter transcriptional activity even in the absence of the viral transactivator Tat. In this work we demonstrate that IRF-1 is also required for full NF-κB transcriptional activity. We provide evidence that IRF-1 and NF-κB form a functional complex at the long terminal repeat (LTR) κB sites, which is abolished by specific mutations in the two adjacent κB sites in the enhancer region. Silencing IRF-1 with small interfering RNA resulted in impaired NF-κB-mediated transcriptional activity and in repressed HIV-1 transcription early in de novo-infected T cells. These data indicate that in early phases of HIV-1 infection or during virus reactivation from latency, when the viral transactivator is absent or present at very low levels, IRF-1 is an additional component of the p50/p65 heterodimer binding the LTR enhancer, absolutely required for efficient HIV-1 replication. [ABSTRACT FROM AUTHOR]

Published
2008
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27. IFN regulatory factor-1 negatively regulates CD4+ CD25+ regulatory T cell differentiation by repressing Foxp3 expression.

Author

Fragale A, Gabriele L, Stellacci E, Borghi P, Perrotti E, Ilari R, Lanciotti A, Remoli AL, Venditti M, Belardelli F, and Battistini A

Subjects
Animals, CD4-Positive T-Lymphocytes cytology, Cells, Cultured, Consensus Sequence, Down-Regulation, Forkhead Transcription Factors genetics, Humans, Interferon Regulatory Factor-1 deficiency, Interferon Regulatory Factor-1 genetics, Mice, Mice, Knockout, Promoter Regions, Genetic genetics, Protein Binding, Transcription, Genetic genetics, CD4-Positive T-Lymphocytes immunology, CD4-Positive T-Lymphocytes metabolism, Cell Differentiation immunology, Forkhead Transcription Factors metabolism, Interferon Regulatory Factor-1 metabolism, Interleukin-2 Receptor alpha Subunit immunology
Abstract

Regulatory T (Treg) cells are critical in inducing and maintaining tolerance. Despite progress in understanding the basis of immune tolerance, mechanisms and molecules involved in the generation of Treg cells remain poorly understood. IFN regulatory factor (IRF)-1 is a pleiotropic transcription factor implicated in the regulation of various immune processes. In this study, we report that IRF-1 negatively regulates CD4(+)CD25(+) Treg cell development and function by specifically repressing Foxp3 expression. IRF-1-deficient (IRF-1(-/-)) mice showed a selective and marked increase of highly activated and differentiated CD4(+)CD25(+)Foxp3(+) Treg cells in thymus and in all peripheral lymphoid organs. Furthermore, IRF-1(-/-) CD4(+)CD25(-) T cells showed extremely high bent to differentiate into CD4(+)CD25(+)Foxp3(+) Treg cells, whereas restoring IRF-1 expression in IRF-1(-/-) CD4(+)CD25(-) T cells impaired their differentiation into CD25(+)Foxp3(+) cells. Functionally, both isolated and TGF-beta-induced CD4(+)CD25(+) Treg cells from IRF-1(-/-) mice exhibited more increased suppressive activity than wild-type Treg cells. Such phenotype and functional characteristics were explained at a mechanistic level by the finding that IRF-1 binds a highly conserved IRF consensus element sequence (IRF-E) in the foxp3 gene promoter in vivo and negatively regulates its transcriptional activity. We conclude that IRF-1 is a key negative regulator of CD4(+)CD25(+) Treg cells through direct repression of Foxp3 expression.

Published
2008
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