Results
| PMID | 20713416 |
| Gene Name | CFL1 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 60 |
| Population details | 60 (30 patients with advanced ovarian EMs (ESCs, Stromal Cells of eutopic endometria in Endometriosis patients), 30 control patients without EMs (NSCs, Stromal Cells of eutopic endometria in Non-endometriosis patients)) |
| Sex | Female |
| Associated genes | CFL1 |
| Other associated phenotypes |
Endometriosis |
|
Hum Reprod. 2010 Oct;25(10):2480-8. doi: 10.1093/humrep/deq197. Epub 2010 Aug 16. Xu, Yan-Li| Wang, Dan-Bo| Liu, Qi-Fang| Chen, Ying-Han| Yang, Zhuo Department of Obstetrics and Gynaecology, Shengjing Hospital, China Medical University, 36 Sanhao Street, Shenyang 110004, China. BACKGROUND: Eutopic endometria with endometriosis (EMs) differ dramatically from normal endometria, physiologically and biochemically, yet the pathogenesis of EMs remains unclear. Cofilin-1 (CFL1), 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 CFL1 than normal endometria, the effects of CFL1 on the pathogenesis of EMs are unknown. The aim of this study was to explore the role of CFL1 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 CFL1 gene in ESCs, and pEGFP-N1-CFL recombinant plasmid was transiently transfected into NSCs to up-regulate CFL1 expression. RESULTS: Under basal conditions, CFL1 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 CFL1 gene in ESCs markedly attenuated proliferation, adhesion, invasion and expression of the markers, but enhanced apoptosis. Conversely, up-regulation of CFL1 in NSCs increased proliferation, adhesion, invasion and expression of the markers but reduced apoptosis. CONCLUSIONS: The overexpression of CFL1 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 CFL1 gene silencing with shRNA interference. Mesh Terms: Adult| Apoptosis| Cell Adhesion| Cell Movement| Cell Proliferation| Cell Survival| Cofilin 1/*genetics| Endometriosis/*metabolism/pathology| Endometrium/*metabolism/ultrastructure| Female| *Gene Silencing| Humans| Middle Aged| Neovascularizat |
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