Up-regulation of IRF-3 expression through GATA-1 acetylation by histone deacetylase inhibitor in lung adenocarcinoma A549 cells

Oncotarget
Lu-Lu WangGuo-Ping Zhou

Abstract

Interferon regulatory factor 3 (IRF-3) is an important transcription factor for interferon genes. Although its functional activation by viral infection has been widely explicated, the regulatory mechanism of IRF-3 gene expression in cancer cells is poorly understood. In this study, we demonstrated treatment of lung adenocarcinoma A549 cells with trichostatin A (TSA) and valproic acid (VPA), two different classes of histone deacetylase inhibitors, strongly stimulated IRF-3 gene expression. Truncated and mutated IRF-3 promoter indicated that a specific GATA-1 element was responsible for TSA-induced activation of IRF-3 promoter. Chromatin immunoprecipitation and electrophoretic mobility shift assay showed that TSA treatment increased the binding affinity of GATA-1 to IRF-3 promoter. Using immunoprecipitation assay and immunoblotting, we demonstrated that TSA increased the level of acetylated GATA-1 in A549 cells. In summary, our study implied that TSA enhanced IRF-3 gene expression through increased GATA-1 recruitment to IRF-3 promoter and the acetylation level of GATA-1 in lung adenocarcinoma A549 cells.

References

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Oct 6, 2016·Oncotarget·Kol Jia YongLi Chai

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Citations

May 16, 2018·Dose-response : a Publication of International Hormesis Society·Lina ŠlekienėAngelija Valančiūtė

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Methods Mentioned

BETA
acetylation
immunoprecipitation
electrophoresis
electrophoretic mobility shift
ChIP
surgical resection
PCR
transfection
Assay
Protein Assay

Software Mentioned

AliBaba2
Matlnspector

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