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Article

Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells

  • Authors:
    • Yu Chen
    • Shengyun Cai
    • Jingwen Wang
    • Mingjuan Xu
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynaecology, Changhai Hospital, The Second Military Medical University, Shanghai 200433, P.R. China
  • Pages: 725-732
    |
    Published online on: June 29, 2015
       https://doi.org/10.3892/ijmm.2015.2263
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Abstract

Endometriosis is a common type of estrogen‑dependent, gynecological and chronic inflammatory disease. Epigenetics refers to changes in gene expression that occur without altering the DNA sequence or DNA content. Histone modification dominates epigenetics, and histone acetylation is the most extensively studied type of histone modification. The CYP19 gene is the gene that encodes P450 aromatase, which regulates the synthesis of estrogen. Hence, we conducted this study to investigate whether histone acetylation has an effect on CYP19 expression and whether histone acetylation is related to endometrial stromal cells (ESCs). Reverse transcription-quantitative polymerase chain reaction (RT‑qPCR), western blot analysis and chromatin immunoprecipitation assays were performed. The results revealed that valproic acid (VPA) significantly promoted histone acetylation in the ESCs, which inhibited histone acetylation in the promoter region of the CYP19 gene, thus suppressing its expression. We also noted that VPA inhibited cell viability and proliferation, and induced the apoptosis, of ESCs. The findings of our study on histone acetylation, endometriosis and the CYP19 gene provide insight which may aid in the research of histone acetylation and suggest that the CYP19 gene may be a novel therapeutic target and method for the treatment of endometriosis.
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Copy and paste a formatted citation
Spandidos Publications style
Chen Y, Cai S, Wang J and Xu M: Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells. Int J Mol Med 36: 725-732, 2015.
APA
Chen, Y., Cai, S., Wang, J., & Xu, M. (2015). Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells. International Journal of Molecular Medicine, 36, 725-732. https://doi.org/10.3892/ijmm.2015.2263
MLA
Chen, Y., Cai, S., Wang, J., Xu, M."Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells". International Journal of Molecular Medicine 36.3 (2015): 725-732.
Chicago
Chen, Y., Cai, S., Wang, J., Xu, M."Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells". International Journal of Molecular Medicine 36, no. 3 (2015): 725-732. https://doi.org/10.3892/ijmm.2015.2263
Copy and paste a formatted citation
x
Spandidos Publications style
Chen Y, Cai S, Wang J and Xu M: Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells. Int J Mol Med 36: 725-732, 2015.
APA
Chen, Y., Cai, S., Wang, J., & Xu, M. (2015). Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells. International Journal of Molecular Medicine, 36, 725-732. https://doi.org/10.3892/ijmm.2015.2263
MLA
Chen, Y., Cai, S., Wang, J., Xu, M."Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells". International Journal of Molecular Medicine 36.3 (2015): 725-732.
Chicago
Chen, Y., Cai, S., Wang, J., Xu, M."Valproic acid-induced histone acetylation suppresses CYP19 gene expression and inhibits the growth and survival of endometrial stromal cells". International Journal of Molecular Medicine 36, no. 3 (2015): 725-732. https://doi.org/10.3892/ijmm.2015.2263
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