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Trichostatin A, a Histone Deacetylase Inhibitor, Attenuates Invasiveness and Reactivates E-Cadherin Expression in Immortalized Endometriotic Cells

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Abstract

The objective of this study is to determine whether trichostatin A (TSA) can suppress the invasiveness of 2 endometriotic cell lines known to be invasive and E-cadherin negative. The membrane invasion culture system was used to assess cell invasion using invasive and a noninvasive bladder cancer cell lines as positive and negative controls, respectively. The E-cadherin mRNA levels and protein expression were evaluated by real-time reverse transcriptase polymerase chain reaction and Western blot analysis, respectively. The authors found that TSA attenuates the invasiveness of 2 cell lines in the presence or absence of tumor necrosis factor α (TNFα) stimulation. In addition, TSA treatment reactivates E-cadherin gene and protein expression in these cell lines. These results, along with recent findings that TSA suppresses proliferation, interleukin-1β—induced cyclo-oxygenase 2 expression, and constitutive or TNFα-stimulated nuclear factor κ B activation in endometrial and endometriotic cells, makes histone deacetylase inhibitors a promising class of compounds for novel and more effective medical treatment of endometriosis, especially given the mounting evidence that endometrios be an epigenetic disease.

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Correspondence to Sun-Wei Guo PhD.

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Financial support was provided by The Children’s Research Institute, Milwaukee, Wisconsin. We thank Alexander Schreiner for critical reading of the article, Monika Kamprad for expert technical assistance, and 2 anonymous reviewers for their constructive comments on an earlier version of the article.

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Wu, Y., Starzinski-Powitz, A. & Guo, SW. Trichostatin A, a Histone Deacetylase Inhibitor, Attenuates Invasiveness and Reactivates E-Cadherin Expression in Immortalized Endometriotic Cells. Reprod. Sci. 14, 374–382 (2007). https://doi.org/10.1177/1933719107302913

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