Abstract
PurposeRecent studies have demonstrated the differential expression of micro(mi)RNAs in endometriosis. Previously, we reported the low expression of miR-141 in patients with this disease. Epithelial-to-mesenchymal transition (EMT) and the transforming growth factor-beta1 (TGF-β1)-induced SMAD2 signalling pathway are central to tumour proliferation and invasion. However, the role of miR-141 in regulating the TGF-β1/SMAD2 signalling pathway and the associated EMT to be elucidated.MethodsThe levels of TGF-β1/SMAD2 signalling and EMT markers expression in eutopic and ectopic endometria of endometriosis were determined by immunohistochemistry and western blot analyses. MiR-141 expression was analysed by quantitative reverse-transcription polymerase chain reaction. Cellular invasion and proliferation were determined by transwell and CCK-8 assays, respectively. Functional assay of miR-141 was performed using plasmid and shRNA transfection methods.ResultThe presence of miR-141, EMT, and TGF-β1/SMAD2 signalling markers were detected in eutopic and ectopic endometria of endometriosis. TGF-β1-induced EMT in Ishikawa (ISK) cells by activating the SMAD2 signalling pathway, whereas miR-141 inhibited the TGF-β1-induced EMT, proliferation and invasion abilities of these cells.ConclusionThese data identify miR-141 as a novel driver of EMT in endometriosis, implicates the link between miR-141 and TGF-β1/SMAD2 signalling pathway in the context of endometriosis, and underscore the role of EMT in the development of endometriosis.
Highlights
Endometriosis is a condition in which endometrial cells grow outside the uterus, causing infertility and pelvic pain in women, affecting 6–10% of women of reproductive age [1, 2]
Abnormal Epithelial-to-mesenchymal transition (EMT) and TGF‐β1/SMAD2 signalling pathway‐related molecules expression were observed in endometriosis
To investigate the involvement of EMT and TGF-β1/ SMAD2 signalling pathway in the development of endometriosis, IHC and western blot analyses of E-cadherin, vimentin, TGF-β1, SMAD2, and phospho-SMAD2 expression were performed on eutopic and ectopic endometria of endometriosis and on normal endometrial tissue
Summary
Endometriosis is a condition in which endometrial cells grow outside the uterus, causing infertility and pelvic pain in women, affecting 6–10% of women of reproductive age [1, 2]. Endometriosis is considered benign gynecological disease, it has cancer-like features as it can recapitulate certain features of malignant neoplasms, including migration and resistance to apoptosis [3, 4]. EMT is considered an essential process associated with cancer metastasis and invasion. TGF-β from the inflammatory tumour microenvironment may induce either tumour cell apoptosis and cancer suppression or induce an EMT to promote tumour cell invasion and metastasis [10, 11]. TGF-β is a principal component of the signalling associated with endometriosis; for instance, the activity of TGF-β1 is increased in the peritoneal fluid of women with this condition [7, 12].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
