microRNA-141 inhibits TGF-β1-induced epithelial-to-mesenchymal transition through inhibition of the TGF-β1/SMAD2 signalling pathway in endometriosis.

Recent 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. The 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. The 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. These 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.

Citation

Sixue Wang, Mengmeng Zhang, Tingting Zhang, Juan Deng, Xiaomeng Xia, Xiaoling Fang. microRNA-141 inhibits TGF-β1-induced epithelial-to-mesenchymal transition through inhibition of the TGF-β1/SMAD2 signalling pathway in endometriosis. Archives of gynecology and obstetrics. 2020 Mar;301(3):707-714

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PMID: 31903498

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