Trichostatin A, a histone deacetylase inhibitor, attenuates invasiveness and reactivates E-cadherin expression in immortalized endometriotic cells.

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 alpha (TNFalpha) 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 beta-induced cyclo-oxygenase 2 expression, and constitutive or TNFalpha-stimulated nuclear factor kappa 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.