Trichostatin A, a Histone Deacetylase Inhibitor, Attenuates Invasiveness and Reactivates E-Cadherin Expression in Immortalized Endometriotic Cells
Trichostatin A, a histone deacetylase inhibitor, reduces invasiveness and restores E-cadherin expression in immortalized endometriotic cells.
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This study tested whether the histone deacetylase inhibitor trichostatin A (TSA) could suppress invasiveness in two invasive, E-cadherin–negative immortalized endometriotic cell lines, using a membrane invasion culture system with bladder cancer cell lines as positive and negative controls. TSA treatment reduced invasiveness in both cell lines in the presence or absence of TNFα and reactivated E-cadherin expression at both mRNA and protein levels, measured by real-time RT-PCR and Western blotting. The authors present their results alongside prior findings that TSA inhibits proliferation and COX-2 and modulates NF-κB activity in endometrial/endometriotic cells, framing epigenetic effects as a rationale. A key caveat is that the work is confined to in vitro models and reports these outcomes without defining the precise epigenetic mechanism linking TSA to E-cadherin re-expression. This paper is centrally about endometriosis — TSA’s ability to attenuate invasiveness and restore E-cadherin expression in immortalized endometriotic cells.
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