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12 results on '"DI LEONARDO E"'

1. The sensitization of HepG2 and HT29 cells to TRAIL-induced apoptosis by histone deacetylase inhibitors is mediated by down-regulation of AKT and NF-kB

Author

EMANUELE, Sonia, LAURICELLA, Marianna, D'ANNEO, Antonella, CARLISI, Daniela, DI FAZIO, Pietro, ANGILERI, Liliana, CIRAOLO, Anna, VENTO, Renza, DI LEONARDO E, TESORIERE G., EMANUELE S, LAURICELLA M, D'ANNEO A, CARLISI D, Di FAZIO P, DI LEONARDO E, ANGILERI L, CIRAOLO A, VENTO R, and TESORIERE G

Subjects
Hepatoma cells, TRAIL, HDACI
Published
2008

4. Differentiative pathway activated by 3-aminobenzamide, an inhibitor of PARP, in human osteosarcoma MG-63 cells

Author

De Blasio, A., Messina, C., Santulli, A., Mangano, V., Di Leonardo, E., D’Anneo, A., Tesoriere, G., and Vento, R.

Subjects
OSTEOSARCOMA, CELLS, GENE expression, OSTEOPONTIN
Abstract

Abstract: This study describes the molecular mechanism by which treatment with 3-AB, a potent inhibitor of PARP, allows human osteosarcoma MG-63 cells to restrict growth and enter differentiation. Our findings show that in MG-63 cells, aberrant gene expression keeps Rb protein constitutively inactivated through hyperphosphorylation and this promotes uncontrolled proliferation of the cells. After 3-AB-treatment, the poly(ADP-ribosyl)ation of nuclear proteins markedly decreases and this results in an increase in both the hypophosphorylated active form of Rb and pRb/E2F complexes. These effects are accompanied by G1 arrest, downregulation of gene products required for proliferation (cyclin D1, β-catenin, c-Jun, c-Myc and Id2) and upregulation of those implicated in the osteoblastic differentiation (p21/Waf1, osteopontin, osteocalcin, type I collagen, N-cadherins and alkaline phosphatase). Our study suggests that use of PARP inhibitors may induce a remodeling of chromatin with the reprogramming of gene expression and the activation of differentiation. [Copyright &y& Elsevier]

Published
2005
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5. Differentiative pathway activated by 3-aminobenzamide, an inhibitor of PARP, in human osteosarcoma MG-63 cells

Author

Concetta Maria Messina, Andrea Santulli, E. Di Leonardo, Antonella D'Anneo, Giovanni Tesoriere, V. Mangano, A. De Blasio, Renza Vento, DE BLASIO A, MESSINA C, SANTULLI A, MANGANO V, DI LEONARDO E, D'ANNEO A, TESORIERE G, and VENTO R

Subjects
Blotting, Western, Biophysics, Hyperphosphorylation, Cell Cycle Proteins, Poly(ADP-ribose) Polymerase Inhibitors, Cell cycle, Retinoblastoma Protein, Biochemistry, PARP, Rb protein, Cyclin D1, Downregulation and upregulation, Structural Biology, Cell Line, Tumor, Gene expression, Genetics, Humans, Immunoprecipitation, Osteopontin, Enzyme Inhibitors, Phosphorylation, E2F, Molecular Biology, DNA Primers, Adenosine Diphosphate Ribose, Osteosarcoma, Base Sequence, biology, Reverse Transcriptase Polymerase Chain Reaction, G1 Phase, Cell Differentiation, Cell Biology, Flow Cytometry, 3-AB, E2F Transcription Factors, Chromatin, DNA-Binding Proteins, Gene Expression Regulation, Differentiation, Benzamides, biology.protein, Cancer research, Transcription Factors
Abstract

This study describes the molecular mechanism by which treatment with 3-AB, a potent inhibitor of PARP, allows human osteosarcoma MG-63 cells to restrict growth and enter differentiation. Our findings show that in MG-63 cells, aberrant gene expression keeps Rb protein constitutively inactivated through hyperphosphorylation and this promotes uncontrolled proliferation of the cells. After 3-AB-treatment, the poly(ADP-ribosyl)ation of nuclear proteins markedly decreases and this results in an increase in both the hypophosphorylated active form of Rb and pRb/E2F complexes. These effects are accompanied by G1 arrest, downregulation of gene products required for proliferation (cyclin D1, β-catenin, c-Jun, c-Myc and Id2) and upregulation of those implicated in the osteoblastic differentiation (p21/Waf1, osteopontin, osteocalcin, type I collagen, N-cadherins and alkaline phosphatase). Our study suggests that use of PARP inhibitors may induce a remodeling of chromatin with the reprogramming of gene expression and the activation of differentiation.

Published
2004

6. Histone deacetylase inhibitors induce in human hepatoma HepG2 cells acetylation of p53 and histones in correlation with apoptotic effects

Author

B. Vassallo, Daniela Carlisi, P. Di Fazio, Sonia Emanuele, Renza Vento, E. Di Leonardo, Antonella D'Anneo, Giovanni Tesoriere, Marianna Lauricella, CARLISI, D, VASSALLO, B, LAURICELLA, M, EMANUELE, S, D'ANNEO, A, DI LEONARDO, E, DI FAZIO, P, VENTO, R, and TESORIERE, G

Subjects
Cancer Research, Programmed cell death, Carcinoma, Hepatocellular, medicine.drug_class, Antineoplastic Agents, Apoptosis, Biology, Hydroxamic Acids, Histones, Cell Line, Tumor, Settore BIO/10 - Biochimica, medicine, Humans, Benzothiazoles, Enzyme Inhibitors, RNA, Small Interfering, Histone Acetyltransferases, Vorinostat, Histone deacetylase inhibitors, acetylation, p53, histones, apoptosis, hepatoma cells, Liver Neoplasms, Histone deacetylase inhibitor, Acetylation, Proto-Oncogene Proteins c-mdm2, Molecular biology, Histone Deacetylase Inhibitors, Trichostatin A, Histone, Oncology, PCAF, biology.protein, Histone deacetylase, Tumor Suppressor Protein p53, DNA Damage, Toluene, medicine.drug
Abstract

This report shows that histone deacetylase inhibitors (HDACIs) induced apoptosis in human hepatoma HepG2 cells in a dose- and time-dependent manner. Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4. It was observed that HDACIs rapidly induced acetylation of these proteins, being the effects clearly visible already at 30 min of treatment at the same doses which caused apoptosis. Analysis of the immunocomplexes, obtained from nuclear extracts using an antibody against p53, revealed the presence of acetylated p53 together with acetylated forms of histones and histone acetyltransferases p300 and PCAF. Experiments performed using pifithrin-alpha, a reversible inhibitor of p53, showed a correlation between acetylation of p53 and induction of apoptosis. In addition treatment with siRNA against p53 indicated that p53 is involved in the acetylation of histones. In conclusion, this report suggests that complexes constituted by acetylated p53, acetylated histones and coactivators can play a central role in HDACI-induced apoptosis in HepG2 cells.

Published
2008

7. HISTONE DEACETYLASE INHIBITORS SENSITIZE HEPATOMA CELLS TO TRAIL_INDUCED APOPTOSIS

Author

EMANUELE, Sonia, LAURICELLA, Marianna, D'ANNEO, Antonella, CARLISI, Daniela, DI FAZIO, Pietro, ROCCA L, VENTO, Renza, TESORIERE, Giovanni, DI LEONARDO, Elvira Rosalia, OLIVIERI, Melania, EMANUELE S, LAURICELLA M, D'ANNEO A, CARLISI D, DI FAZIO P, DI LEONARDO E, OLIVIERI M, ROCCA L, VENTO R, and TESORIERE

Subjects
HDACI HEPATOMA APOPTOSIS
Published
2008

9. In Human Retinoblastoma Y-79 Cells 3-aminobenzamide induces Differentiation

Author

MANGANO, Valentina, DI LEONARDO, Elvira Rosalia, DE BLASIO, Anna, DRAGO FERRANTE, Rosa, DI FIORE, Riccardo, AUGELLO, Giuseppa, MESSINA, Concetta Maria, SANTULLI, Andrea, VENTO, Renza, Mangano, V, Di Leonardo, E, De Blasio, A, Drago Ferrante, R, Di Fiore, R, Augello, G, Messina, C, Santulli, A, and Vento, R.

Subjects
PARP inhibitor, Retinoblastoma, differentiation
Published
2006

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