Increased Egr-1 binding to promoter induced by histone hyperacetylation promotes gdnf gene transcription / 南方医科大学学报
Journal of Southern Medical University
;
(12): 697-701, 2015.
Artigo
em Chinês
| WPRIM
| ID: wpr-355301
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of high transcription of the glial cell-line derived neurotrophic factor (gdnf) gene induced by hyperacetylation of histone H3 lysine 9 (H3K9) at its promoter region II in rat C6 glioma cells.</p><p><b>METHODS</b>The acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and the binding capacity of Egr-1 to its binding site in gdnf promoter were examined by ChIP-PCR in C6 astroglioma cells and normal rat astrocytes, and its changes were investigated in C6 astroglioma cells after treatment with histone acetyltransferase inhibitor curcumin or deacetylase inhibitor trichostatin A.</p><p><b>RESULTS</b>Compared normal astrocytes, C6 astroglioma cells showed significantly increased acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and Egr-1 binding capacity (P<0.01). Curcumin treatment significantly reduced H3K9 acetylation level at Egr-1 binding site and decreased both the binding of Egr-1 to promoter region II and gdnf mRNA levels in C6 astroglioma cells (P<0.05). Conversely, increased H3K9 acetylation at the Egr-1 binding site induced by trichostatin A significantly increased the binding of Egr-1 to promoter region II and gdnf mRNA expression levels (P<0.05).</p><p><b>CONCLUSION</b>H3K9 hyperacetylation induces increased Egr-1 binding to gdnf gene promoter II, which might be the reason for the high transcription level of gdnf gene in rat C6 glioma cells.</p>
Texto completo:
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Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Acetilação
/
Transcrição Gênica
/
Sítios de Ligação
/
RNA Mensageiro
/
Histonas
/
Química
/
Processamento de Proteína Pós-Traducional
/
Astrócitos
/
Regiões Promotoras Genéticas
/
Linhagem Celular Tumoral
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2015
Tipo de documento:
Artigo
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