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17 results on '"Ferrari, Karin"'

1. WNT Oncogenic Transcription Requires MYC Suppression of Lysosomal Activity and EPCAM Stabilization in Gastric Tumors

Author

Mulè, Patrizia, Fernandez-Perez, Daniel, Amato, Simona, Manganaro, Daria, Oldani, Paola, Brandini, Stefania, Diaferia, Giuseppe, Cuomo, Alessandro, Recordati, Camilla, Soriani, Chiara, Dondi, Ambra, Zanotti, Marika, Rustichelli, Samantha, Bisso, Andrea, Pece, Salvatore, Rodighiero, Simona, Natoli, Gioacchino, Amati, Bruno, Ferrari, Karin Johanna, Chiacchiera, Fulvio, and Pasini, Diego

Published
2024
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3. Increased Lactate Secretion by Cancer Cells Sustains Non-cell-autonomous Adaptive Resistance to MET and EGFR Targeted Therapies

Author

Apicella, Maria, Giannoni, Elisa, Fiore, Stephany, Ferrari, Karin Johanna, Fernández-Pérez, Daniel, Isella, Claudio, Granchi, Carlotta, Minutolo, Filippo, Sottile, Antonino, Comoglio, Paolo Maria, Medico, Enzo, Pietrantonio, Filippo, Volante, Marco, Pasini, Diego, Chiarugi, Paola, Giordano, Silvia, and Corso, Simona

Published
2018
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8. Focal adhesion kinase depletion reduces human hepatocellular carcinoma growth by repressing enhancer of zeste homolog 2

Author

Gnani, Daniela, Romito, Ilaria, Artuso, Simona, Chierici, Marco, De Stefanis, Cristiano, Panera, Nadia, Crudele, Annalisa, Ceccarelli, Sara, Carcarino, Elena, D'Oria, Valentina, Porru, Manuela, Giorda, Ezio, Ferrari, Karin, Miele, Luca, Villa, Erica, Balsano, Clara, Pasini, Diego, Furlanello, Cesare, Locatelli, Franco, Nobili, Valerio, Rota, Rossella, Leonetti, Carlo, Alisi, Anna, Miele, Luca (ORCID:0000-0003-3464-0068), Locatelli, Franco (ORCID:0000-0002-7976-3654), Gnani, Daniela, Romito, Ilaria, Artuso, Simona, Chierici, Marco, De Stefanis, Cristiano, Panera, Nadia, Crudele, Annalisa, Ceccarelli, Sara, Carcarino, Elena, D'Oria, Valentina, Porru, Manuela, Giorda, Ezio, Ferrari, Karin, Miele, Luca, Villa, Erica, Balsano, Clara, Pasini, Diego, Furlanello, Cesare, Locatelli, Franco, Nobili, Valerio, Rota, Rossella, Leonetti, Carlo, Alisi, Anna, Miele, Luca (ORCID:0000-0003-3464-0068), and Locatelli, Franco (ORCID:0000-0002-7976-3654)

Abstract

Hepatocellular carcinoma (HCC) is the most common type of liver cancer in humans. The focal adhesion tyrosine kinase (FAK) is often over-expressed in human HCC and FAK inhibition may reduce HCC cell invasiveness. However, the anti-oncogenic effect of FAK knockdown in HCC cells remains to be clarified. We found that FAK depletion in HCC cells reduced in vitro and in vivo tumorigenicity, by inducing G2/M arrest and apoptosis, decreasing anchorage-independent growth, and modulating the expression of several cancer-related genes. Among these genes, we showed that FAK silencing decreased transcription and nuclear localization of enhancer of zeste homolog 2 (EZH2) and its tri-methylation activity on lysine 27 of histone H3 (H3K27me3). Accordingly, FAK, EZH2 and H3K27me3 were concomitantly upregulated in human HCCs compared to non-tumor livers. In vitro experiments demonstrated that FAK affected EZH2 expression and function by modulating, at least in part, p53 and E2F2/3 transcriptional activity. Moreover, FAK silencing downregulated both EZH2 binding and histone H3K27me3 levels at the promoter of its target gene NOTCH2. Finally, we found that pharmacological inhibition of FAK activity resembled these effects although milder. In summary, we demonstrate that FAK depletion reduces HCC cell growth by affecting cancer-promoting genes including the pro-oncogene EZH2. Furthermore, we unveil a novel unprecedented FAK/EZH2 crosstalk in HCC cells, thus identifying a targetable network paving the way for new anticancer therapies.

Published
2017

9. Focal adhesion kinase depletion reduces human hepatocellular carcinoma growth by repressing enhancer of zeste homolog 2

Author

Gnani, Daniela, primary, Romito, Ilaria, additional, Artuso, Simona, additional, Chierici, Marco, additional, De Stefanis, Cristiano, additional, Panera, Nadia, additional, Crudele, Annalisa, additional, Ceccarelli, Sara, additional, Carcarino, Elena, additional, D’Oria, Valentina, additional, Porru, Manuela, additional, Giorda, Ezio, additional, Ferrari, Karin, additional, Miele, Luca, additional, Villa, Erica, additional, Balsano, Clara, additional, Pasini, Diego, additional, Furlanello, Cesare, additional, Locatelli, Franco, additional, Nobili, Valerio, additional, Rota, Rossella, additional, Leonetti, Carlo, additional, and Alisi, Anna, additional

Published
2017
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17. Regulation and function of DNA and histone methylations.

Author

Ferrari KJ and Pasini D

Subjects
Animals, Base Sequence, Humans, Methylation, Transcription, Genetic, DNA Methylation, Epigenesis, Genetic, Histones metabolism
Abstract

Cell type specification, transcription factor binding site selection and transcriptional regulation are specific processes that require a fine regulation that cannot be simply explained by the mere DNA sequence. Similarly, genome stability, damage response as well as genomic imprints and X-chromosome inactivation are all processes that involve an epigenetic level of regulation. This includes the activity of several enzymes that act in concert to "place" or "remove" specific modifications shaping cells epigenomes with posttranslational modifications of histone proteins and modifications of DNA cytosine residues. In this review, we discuss the role of histone and DNA methylation in regulating different cellular processes with a particular emphasis on transcriptional regulation and on the mechanistic insights behind different enzymatic activities with a perspective towards their implications in human diseases.

Published
2013

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