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EnglishThe advantage of Aurora kinase (AK) inhibitors in chronic myeloid leukemia (CML) therapy mostly arises from off-target effects on tyrosine kinase (TK) activity of wild type (wt) or mutated Bcr-Abl proteins which drive the disease resistance to imatinib (IM). We proved that the AK inhibitor MK-0457 induces the growth arrest DNA damage-inducible (Gadd) 45a through recruitment of octamer-binding (Oct)-1 transcription factor at a critical promoter region for gene transcription and covalent modifications of histone H3 (lysine 14 acetylation, lysine 9 de-methylation). Such epigenetic chromatin modifications may depict a general mechanism promoting the re-activation of tumor suppressor genes silenced by Bcr-Abl.
| Titolo: | Gadd45a transcriptional induction elicited by the Aurora kinase inhibitor MK-0457 in Bcr-Abl-expressing cells is driven by Oct-1 transcription factor |
| Autore/i: | MANCINI, MANUELA; LEO, ELISA; ALUIGI, MICHELA; Chiara Marcozzi; BORSI, ENRICA; BARBIERI, ENZA; SANTUCCI, MARIA ALESSANDRA |
| Autore/i Unibo: | |
| Anno: | 2012 |
| Rivista: | |
| Digital Object Identifier (DOI): | http://dx.doi.org/10.1016/j.leukres.2012.03.025 |
| Abstract: | The advantage of Aurora kinase (AK) inhibitors in chronic myeloid leukemia (CML) therapy mostly arises from off-target effects on tyrosine kinase (TK) activity of wild type (wt) or mutated Bcr-Abl proteins which drive the disease resistance to imatinib (IM). We proved that the AK inhibitor MK-0457 induces the growth arrest DNA damage-inducible (Gadd) 45a through recruitment of octamer-binding (Oct)-1 transcription factor at a critical promoter region for gene transcription and covalent modifications of histone H3 (lysine 14 acetylation, lysine 9 de-methylation). Such epigenetic chromatin modifications may depict a general mechanism promoting the re-activation of tumor suppressor genes silenced by Bcr-Abl. |
| Data prodotto definitivo in UGOV: | 2014-12-12 17:06:48 |
| Appare nelle tipologie: | 1.01 Articolo in rivista |
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