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

Department of Pediatrics, Medical College of Wisconsin, Milwaukee

Anna Starzinski-Powitz, PhD

Molecular Cell Biology and Human Genetics in Biosciences, Johann Wolfgang Goethe University, Frankfurt/Main, Germany

Sun-Wei Guo, PhD

Department of Pediatrics, Medical College of Wisconsin, Milwaukee, swguo{at}mcw.edu

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 (TNF) 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-1 ß—induced cyclo-oxygenase 2 expression, and constitutive or TNF-stimulated nuclear factor 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.

Key Words: Cell line • E-cadherin,endometriotic cell • endometriosis • epigenetics • histone deacetylase inhibitor • invasion • trichostatin A.

Reproductive Sciences, Vol. 14, No. 4, 374-382 (2007)
DOI: 10.1177/1933719107302913


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