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Start Over Author "Soddu, Silvia" Journal cancer research
5 results on '"Soddu, Silvia"'

2. Negative Regulation of β4 Integrin Transcription by Homeodomain-Interacting Protein Kinase 2 and p53 Impairs Tumor Progression

Author

Bon, Giulia, primary, Di Carlo, Selene E., additional, Folgiero, Valentina, additional, Avetrani, Paolo, additional, Lazzari, Chiara, additional, D'Orazi, Gabriella, additional, Brizzi, Maria Felice, additional, Sacchi, Ada, additional, Soddu, Silvia, additional, Blandino, Giovanni, additional, Mottolese, Marcella, additional, and Falcioni, Rita, additional

Published
2009
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3. Identification of an Aberrantly Spliced Form of HDMX in Human Tumors: A New Mechanism for HDM2 Stabilization

Author

Giglio, Simona, primary, Mancini, Francesca, additional, Gentiletti, Francesca, additional, Sparaco, Giorgia, additional, Felicioni, Lara, additional, Barassi, Fabio, additional, Martella, Carla, additional, Prodosmo, Andrea, additional, Iacovelli, Stefano, additional, Buttitta, Fiamma, additional, Farsetti, Antonella, additional, Soddu, Silvia, additional, Marchetti, Antonio, additional, Sacchi, Ada, additional, Pontecorvi, Alfredo, additional, and Moretti, Fabiola, additional

Published
2005
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5. Negative regulation of beta4 integrin transcription by homeodomain-interacting protein kinase 2 and p53 impairs tumor progression.

Author

Bon G, Di Carlo SE, Folgiero V, Avetrani P, Lazzari C, D'Orazi G, Brizzi MF, Sacchi A, Soddu S, Blandino G, Mottolese M, and Falcioni R

Subjects
Blotting, Western, Breast Neoplasms genetics, Breast Neoplasms metabolism, Breast Neoplasms pathology, Carrier Proteins genetics, Cell Line, Tumor, Cell Proliferation, Cytoplasm metabolism, Disease Progression, Female, Gene Expression Regulation, Neoplastic, HCT116 Cells, HT29 Cells, Histone Acetyltransferases metabolism, Humans, Immunohistochemistry, Integrin beta4 genetics, Mitogen-Activated Protein Kinases metabolism, Mutation, Neoplasms genetics, Neoplasms metabolism, Phosphorylation, Protein Serine-Threonine Kinases genetics, Proto-Oncogene Proteins c-akt metabolism, Reverse Transcriptase Polymerase Chain Reaction, Transcription, Genetic, Tumor Suppressor Protein p53 genetics, p300-CBP Transcription Factors metabolism, Carrier Proteins metabolism, Integrin beta4 metabolism, Neoplasms pathology, Protein Serine-Threonine Kinases metabolism, Tumor Suppressor Protein p53 metabolism
Abstract

Increased expression of alpha(6)beta(4) integrin in several epithelial cancers promotes tumor progression; however, the mechanism underlying its transcriptional regulation remains unclear. Here, we show that depletion of homeodomain-interacting protein kinase 2 (HIPK2) activates beta(4) transcription that results in a strong increase of beta(4)-dependent mitogen-activated protein kinase and Akt phosphorylation, anchorage-independent growth, and invasion. In contrast, stabilization of HIPK2 represses beta(4) expression in wild-type p53 (wtp53)-expressing cells but not in p53-null cells or cells expressing mutant p53, indicating that HIPK2 requires a wtp53 to inhibit beta(4) transcription. Consistent with our in vitro findings, a strong correlation between beta(4) overexpression and HIPK2 inactivation by cytoplasmic relocalization was observed in wtp53-expressing human breast carcinomas. Under loss of function of HIPK2 or p53, the p53 family members TAp63 and TAp73 strongly activate beta(4) transcription. These data, by revealing that beta(4) expression is transcriptionally repressed in tumors by HIPK2 and p53 to impair beta(4)-dependent tumor progression, suggest that loss of p53 function favors the formation of coactivator complex with the TA members of the p53 family to allow beta(4) transcription.

Published
2009
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