BM88/Cend1 is involved in histone deacetylase inhibition-mediated growth arrest and differentiation of neuroblastoma cells

• Published in: FEBS letters Vol. 582; no. 5; pp. 741 - 748
• Main Authors: Politis, Panagiotis K., Akrivou, Sofia, Hurel, Catherine, Papadodima, Olga, Matsas, Rebecca
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 05.03.2008
• Subjects: Acetylation; Animals; Cell Differentiation - drug effects; Cell Proliferation - drug effects; Gene Expression Regulation, Neoplastic - drug effects; Histone Deacetylase Inhibitors; Hydroxamic Acids - pharmacology; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Neuroblastoma - enzymology; Neuroblastoma - pathology; Neurons - drug effects; Neurons - pathology; NIH 3T3 Cells; Proliferation; Promoter activation; Promoter Regions, Genetic - genetics; Protein Biosynthesis - drug effects; Repressor Proteins - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; Transcription; Transcription, Genetic - drug effects; Trichostatin-A; Up-Regulation - drug effects; β-III-Tubulin; β-III-Tubulin; Proliferation; Acetylation; Transcription; Promoter activation; Trichostatin-A
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2008.01.052

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.