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BM88/Cend1 is involved in histone deacetylase inhibition‐mediated growth arrest and differentiation of neuroblastoma cells
Author(s) -
Politis Panagiotis K.,
Akrivou Sofia,
Hurel Catherine,
Papadodima Olga,
Matsas Rebecca
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.01.052
Subject(s) - trichostatin a , histone deacetylase , histone deacetylase 5 , hdac11 , gene knockdown , microbiology and biotechnology , cellular differentiation , neuroblastoma , histone , histone deacetylase 2 , chemistry , hdac1 , biology , cell cycle checkpoint , cell growth , cancer research , cell cycle , gene , cell culture , genetics
Histone deacetylase inhibitors arrest the growth of neuroblastoma cells and induce differentiation. Identification of target genes that co‐ordinate and mediate these effects is important for understanding the function of this novel class of antitumour drugs. We report here that trichostatin‐A (TSA) specifically induces the transcription of Cend1 , a neuronal‐lineage specific regulator of cell cycle exit and differentiation, in neuroblastoma Neuro2A cells, but not in non‐neuronal cells. Furthermore, we show that knockdown of Cend1 alleviates both the anti‐proliferative and differentiation effect of TSA. Our findings suggest that Cend1 is an important molecular target for HDAC inhibition.