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41 results on '"Cesi, Vincenzo"'

2. Involvement of Mitochondria in the Selective Response to Microsecond Pulsed Electric Fields on Healthy and Cancer Stem Cells in the Brain

Author

Casciati, Arianna, primary, Taddei, Anna Rita, additional, Rampazzo, Elena, additional, Persano, Luca, additional, Viola, Giampietro, additional, Cani, Alice, additional, Bresolin, Silvia, additional, Cesi, Vincenzo, additional, Antonelli, Francesca, additional, Mancuso, Mariateresa, additional, Merla, Caterina, additional, and Tanori, Mirella, additional

Published
2024
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4. PARP1 Activation Induces HMGB1 Secretion Promoting Intestinal Inflammation in Mice and Human Intestinal Organoids

Author

Vitali, Roberta, primary, Mancuso, Anna Barbara, additional, Palone, Francesca, additional, Pioli, Claudio, additional, Cesi, Vincenzo, additional, Negroni, Anna, additional, Cucchiara, Salvatore, additional, Oliva, Salvatore, additional, Carissimi, Claudia, additional, Laudadio, Ilaria, additional, and Stronati, Laura, additional

Published
2023
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15. RIP3, A Regulator of Necroptosis, Promotes Inflammation by Increasing Cytokine and Inflammasome Molecule Levels as Well as Altering Membrane Permeability in Intestinal Epithelial CellS

Author

Colantoni, Eleonora, primary, Negroni, Anna, additional, Cesi, Vincenzo, additional, Palone, Francesca, additional, Costanzo, Manuela, additional, Viola, Franca, additional, Oliva, Salvatore, additional, Cucchiara, Salvatore, additional, and Stronati, Laura, additional

Published
2017
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26. Slug (SNAI2) Down-Regulation by RNA Interference Facilitates Apoptosis and Inhibits Invasive Growth in Neuroblastoma Preclinical Models

Author

Vitali, Roberta, primary, Mancini, Camillo, additional, Cesi, Vincenzo, additional, Tanno, Barbara, additional, Mancuso, Mariateresa, additional, Bossi, Gianluca, additional, Zhang, Ying, additional, Martinez, Robert V., additional, Calabretta, Bruno, additional, Dominici, Carlo, additional, and Raschellà, Giuseppe, additional

Published
2008
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32. BCR-ABL suppresses C/EBPα expression through inhibitory action of hnRNP E2

Author

Perrotti, Danilo, primary, Cesi, Vincenzo, additional, Trotta, Rossana, additional, Guerzoni, Clara, additional, Santilli, Giorgia, additional, Campbell, Kenneth, additional, Iervolino, Angela, additional, Condorelli, Fabrizio, additional, Gambacorti-Passerini, Carlo, additional, Caligiuri, Michael A., additional, and Calabretta, Bruno, additional

Published
2001
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37. BCR-ABL suppresses C/EBPα expression through inhibitory action of hnRNP E2.

Author

Perrotti, Danilo, Cesi, Vincenzo, Trotta, Rossana, Guerzoni, Clara, Santilli, Giorgia, Campbell, Kenneth, Iervolino, Angela, Condorelli, Fabrizio, Gambacorti-Passerini, Carlo, Caligiuri, Michael A., and Calabretta, Bruno

Subjects
*MYELOID leukemia, *GRANULOCYTE-macrophage colony-stimulating factor
Abstract

The arrest of differentiation is a feature of both chronic myelogenous leukemia cells in myeloid blast crisis and myeloid precursors that ectopically express the p210[sup BCR-ABL] oncoprotein; however, its underlying mechanisms remain poorly understood. Here we show that expression of BCR-ABL in myeloid precursor cells leads to transcriptional suppression of the granulocyte colony-stimulating factor receptor G-CSF-R (encoded by CSF3R), possibly through down-modulation of C/EBPα—the principal regulator of granulocytic differentiation. Expression of C/EBPα protein is barely detectable in primary marrow cells taken from individuals affected with chronic myeloid leukemia in blast crisis. In contrast, CEBPA RNA is clearly present. Ectopic expression of C/EBPα induces granulocytic differentiation of myeloid precursor cells expressing BCR-ABL. Expression of C/EBPα is suppressed at the translational level by interaction of the poly(rC)-binding protein hnRNP E2 with CEBPA mRNA, and ectopic expression of hnRNP E2 in myeloid precursor cells down-regulates both C/EBPα and G-CSF-R and leads to rapid cell death on treatment with G-CSF (encoded by CSF3). Our results indicate that BCR-ABL regulates the expression of C/EBPα by inducing hnRNP E2—which inhibits the translation of CEBPA mRNA. [ABSTRACT FROM AUTHOR]

Published
2002
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39. TGFβ-induced c-Myb affects the expression of EMT-associated genes and promotes invasion of ER+ breast cancer cells.

Author

Cesi V, Casciati A, Sesti F, Tanno B, Calabretta B, and Raschellà G

Subjects
Apoptosis, Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Cadherins genetics, Cadherins metabolism, Cell Line, Tumor, Cell Proliferation, Cloning, Molecular, Epithelial-Mesenchymal Transition, Estrogen Receptor alpha genetics, Estrogen Receptor alpha metabolism, Etoposide pharmacology, Female, Flow Cytometry, Genes, myb, Humans, Lentivirus genetics, Lentivirus metabolism, MicroRNAs genetics, MicroRNAs metabolism, Mutagenesis, Site-Directed, Neoplasm Invasiveness, Protein Processing, Post-Translational, Protein Stability, Proto-Oncogene Proteins c-myb genetics, RNA, Small Interfering genetics, RNA, Small Interfering metabolism, Receptors, Transforming Growth Factor beta genetics, Receptors, Transforming Growth Factor beta metabolism, Transcriptional Activation, Transfection, Breast Neoplasms pathology, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myb metabolism, Transforming Growth Factor beta pharmacology
Abstract

Advanced breast cancer cells acquire metastatic properties in response to TGFβ. We show here that the expression of c-Myb increases in TGFβ-treated ER (+) breast cancer cells by protein stabilization, transcription activation and release from miR200-dependent down-regulation. In particular, we mapped 2 sites for miR200b, miR200c and miR429 binding in the 3' UTR of the human c-myb gene. These microRNAs decreased the expression of c-Myb when transfected in MCF-7 cells. In addition, luciferase activity from a vector containing the 3' UTR of the c-myb gene was inhibited by miR200s through a binding-dependent mechanism. siRNA- and shRNA-mediated down-regulation was used to investigate the role of c-Myb for the effects induced by TGFβ in ER(+) breast cancer MCF-7 and ZR-75.1 cells. Transfection with c-Myb siRNAs blocked the increase of Slug (SNAI2) and Bcl-2 expression and reversed the decrease in E-cadherin expression induced by TGF-β treatment. Conversely, c-Myb down-regulation decreased invasion and anchorage-independent growth of breast cancer cells expressing a constitutively active TGFβ receptor I. Finally, apoptosis induced by etoposide increased in c-Myb-silenced TGFβ-treated ER(+) cell lines. In summary, exposure of ER(+) breast cancer cells to TGFβ induces an increase of c-Myb expression which is required for expression of EMT-associated markers, in vitro invasion and anchorage-independent growth. Furthermore, our findings suggest a potentially detrimental effect of TGFβ and c-Myb co-expression in breast cancer.

Published
2011
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40. C/EBP alpha and beta mimic retinoic acid activation of IGFBP-5 in neuroblastoma cells by a mechanism independent from binding to their site.

Author

Cesi V, Giuffrida ML, Vitali R, Tanno B, Mancini C, Calabretta B, and Raschellà G

Subjects
Base Sequence, CCAAT-Enhancer-Binding Protein-alpha genetics, CCAAT-Enhancer-Binding Protein-beta genetics, Cell Line, Tumor, DNA Primers, Humans, Insulin-Like Growth Factor Binding Protein 5 genetics, Kinetics, Neuroblastoma, Oligonucleotide Probes, Promoter Regions, Genetic, Protein Binding, Reverse Transcriptase Polymerase Chain Reaction, CCAAT-Enhancer-Binding Protein-alpha metabolism, CCAAT-Enhancer-Binding Protein-beta metabolism, Insulin-Like Growth Factor Binding Protein 5 metabolism
Abstract

Signal transduction mediated by insulin-like growth factors is implicated in the aggressive behavior of neuroblastoma (NB), a childhood tumor originating from the neural crest. IGFBP-5, a protein that binds IGFs with high affinity, is expressed in many NB cell lines exerting opposite effects, depending on its concentration. We found that IGFBP-5 expression increased during retinoic acid (RA)-mediated differentiation of NB cells. This was due to transcriptional activation as demonstrated by reporter assays carried out in basal and differentiating conditions. We defined the shortest region of the human IGFBP-5 promoter (from nucleotide -83 to +53) which is sensitive to RA. Mutation of a CCAAT enhancer binding protein (C/EBP) element inside this region increased transcription, suggesting a repressive role of this sequence. DNA Affinity Precipitation Assays (DAPA) and chromatin immunoprecipitation demonstrated that the binding of C/EBPalpha and beta to the C/EBP site decreased upon treatment with RA. C/EBPalpha and beta induced an increase in IGFBP-5 transcription in human and murine NB cells similar to that obtained upon RA treatment. Activation by C/EBP alpha and beta did not depend on their binding to the C/EBP site, since they still activated IGFBP-5 promoter carrying a mutation in the C/EBP site. Of interest, we found that both transcription factors were able to interact with the TATA box, but only C/EBPalpha interaction increased during RA-induced differentiation.

Published
2005
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41. c-Kit is preferentially expressed in MYCN-amplified neuroblastoma and its effect on cell proliferation is inhibited in vitro by STI-571.

Author

Vitali R, Cesi V, Nicotra MR, McDowell HP, Donfrancesco A, Mannarino O, Natali PG, Raschellà G, and Dominici C

Subjects
Benzamides, Cell Division drug effects, Child, Child, Preschool, DNA Primers chemistry, Gene Amplification, Humans, Imatinib Mesylate, Immunoenzyme Techniques, Infant, Infant, Newborn, Neoplasm Staging, Neuroblastoma pathology, Protein-Tyrosine Kinases antagonists & inhibitors, Proto-Oncogene Proteins c-kit genetics, RNA, Messenger genetics, RNA, Messenger metabolism, RNA, Neoplasm metabolism, Reverse Transcriptase Polymerase Chain Reaction, Stem Cell Factor genetics, Tumor Cells, Cultured drug effects, Antineoplastic Agents pharmacology, Gene Expression Regulation, Neoplastic, Genes, myc physiology, Neuroblastoma metabolism, Piperazines pharmacology, Proto-Oncogene Proteins c-kit metabolism, Pyrimidines pharmacology, Stem Cell Factor metabolism
Abstract

Coexpression for c-Kit receptor and its ligand stem cell factor (SCF) has been described in neuroblastoma (NB) cell lines and tumors, suggesting the existence of an autocrine loop modulating tumor growth. We evaluated c-Kit and SCF expression by immunohistochemistry in a series of 75 primary newly diagnosed neuroblastic tumors. Immunostaining for c-Kit was found in 10/75 and for SCF in 17/75, with 5/10 c-Kit-positive tumors also expressing SCF. For both, c-Kit and SCF staining were predominantly found in the most aggressive subset of tumors, i.e., those amplified for MYCN: c-Kit was detected in 8/14 amplified vs. 2/61 single copy (p<0.001), and SCF in 9/14 amplified vs. 8/61 single copy tumors (p<0.001). Furthermore, the association of c-Kit expression with advanced stage (3 or 4) (p=0.001) and of SCF expression with adrenal primary (p=0.03) was substantiated. The in vitro activity of the tyrosine kinase inhibitor STI-571 (imatinib mesylate, Gleevec, Glivec) on NB cell lines positive or negative for c-Kit was also assessed. When cells were grown in 10% fetal calf serum, the 4 c-Kit-positive cell lines tested were sensitive to STI-571 growth inhibition to a different extent (ranging from 30 to 80%); also the c-Kit-negative cell line GI-CA-N was slightly affected, suggesting that other STI-571 targets operate in regulating NB proliferation. In addition, c-Kit-positive cell lines SK-N-BE2(c) and HTLA230, grown in SCF only, remained sensitive (40 and 70% of growth inhibition, respectively), while, in the same conditions, proliferation of the c-Kit-negative cell line GI-CA-N was not affected. Immunoprecipitation of c-Kit from cell lysates of SK-N-BE2(c) and HTLA230 cells grown in SCF and subsequent western blot analysis of the immunoprecipitates revealed a sharp decrease of c-Kit phosphorylation after STI-571 treatment. These data demonstrate that both c-Kit and SCF are preferentially expressed in vivo in the most aggressive neuroblastic tumors and that their signaling is active in promoting in vitro NB cell proliferation that can be selectively inhibited by treatment with STI-571., (Copyright 2003 Wiley-Liss, Inc.)

Published
2003
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