BACKGROUND
Eutopic endometria with endometriosis (EMs) differ dramatically from normal endometria, physiologically and biochemically, yet the pathogenesis of EMs remains unclear. Cofilin-1 (<em>CFL</em>1), a critical modulator of the actin cystoskeleton, is associated with tumour progression, cell motility, cell adhesion, cell invasion and angiogenesis. Although eutopic endometria with EMs exhibit many malignant-like behaviours and a higher expression of <em>CFL</em>1 than normal endometria, the effects of <em>CFL</em>1 on the pathogenesis of EMs are unknown. The aim of this study was to explore the role of <em>CFL</em>1 expression in proliferation, apoptosis, adhesion, invasion, angiogenesis and ultrastructure of endometrial cells.
METHODS
We isolated and cultured stromal cells derived from the eutopic endometria of 30 patients with advanced ovarian EMs (ESCs, Stromal Cells of eutopic endometria in Endometriosis patients) and 30 control patients without EMs (NSCs, Stromal Cells of eutopic endometria in Non-endometriosis patients), and evaluated their proliferation, apoptosis, adhesion, invasion and expression of markers of adhesion, invasion and angiogenesis in vitro. In addition, these functions were examined after short hairpin RNA (shRNA) was used to silence the <em>CFL</em>1 gene in ESCs, and pEGFP-N1-<em>CFL</em> recombinant plasmid was transiently transfected into NSCs to up-regulate <em>CFL</em>1 expression.
RESULTS
Under basal conditions, <em>CFL</em>1 mRNA and protein were overexpressed in ESCs. Proliferation, adhesion, invasion and markers of adhesion, invasion and angiogenesis were enhanced in ESCs compared with NSCs; in contrast, the apoptosis rate was lower in ESCs than in NSCs. Silencing the <em>CFL</em>1 gene in ESCs markedly attenuated proliferation, adhesion, invasion and expression of the markers, but enhanced apoptosis. Conversely, up-regulation of <em>CFL</em>1 in NSCs increased proliferation, adhesion, invasion and expression of the markers but reduced apoptosis.
CONCLUSIONS
The overexpression of <em>CFL</em>1 in ESCs is associated with enhanced proliferation, adhesion, invasion and angiogenesis and reduced apoptosis in EMs. These malignant-like behaviours of ESCs in EMs can be attenuated by inducing <em>CFL</em>1 gene silencing with shRNA interference.