Results
PMID | 25529997 |
Gene Name | LIMK1 |
Condition | Endometriosis |
Association |
Associated |
Population size | 60 |
Population details | 60 (30 patients with endometriosis, 30 patients without endometriosis) |
Sex | Female |
Other associated phenotypes |
Endometriosis |
Cell Tissue Res. 2015 Mar;359(3):885-93. doi: 10.1007/s00441-014-2068-5. Epub Zhang, Zhifang| Chen, Peng| Guo, Cuishan| Meng, Xiannan| Wang, Danbo Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, People's Republic of China. LIM kinase 1 (LIMK1) has been implicated in tumour invasion and migration in several tumour types. However, its role in the progression of endometriosis has not yet been studied. Our aim is to analyse LIMK1 expression in endometriosis-derived stromal cells and to explore the effects of LIMK1 overexpression on their biological behaviour. The mRNA and protein expression levels of LIMK1 of eutopic endometrial stromal cells (ESCs) separated from 30 endometriosis patients and normal endometrial stromal cells (NSCs) separated from 30 patients without endometriosis were analysed by real-time polymerase chain reaction and Western blot. Lentiviral particles containing human LIMK1 short interfering RNA were used to silence the LIMK1 gene in ESCs and LIMK1-expressing lentiviral particles containing the total LIMK1 cDNA was transfected into NSCs to upregulate LIMK1 expression. Cell migration, invasion, proliferation and expression of markers of adhesion, invasion and angiogenesis of ESCs and NSCs were evaluated under basal conditions and after transfection in vitro. The mRNA and protein expression levels of LIMK1 in ESCs were higher than those in NSCs. Under basal conditions, ESCs exhibited greater cell migration, invasion and proliferation and higher levels of markers of adhesion, invasion and angiogenesis than NSCs. The behaviour of ESCs was decreased after LIMK1 gene silencing and that of NSCs was elevated after LIMK1 gene upregulation. Thus, LIMK1 is overexpressed in ESCs thereby facilitating malignant-like behaviour, including enhanced migration, invasion, proliferation and angiogenesis, all of which contribute to the occurrence and development of endometriosis. Mesh Terms: Adult| Cell Movement| Cell Proliferation| Endometriosis/*metabolism/*pathology| Female| Gene Knockdown Techniques| Gene Silencing| Humans| Intercellular Adhesion Molecule-1/metabolism| Lim Kinases/*metabolism| Matrix Metalloproteinase 9/secretio |