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Publication : MicroRNA-30a-3p regulates epithelial-mesenchymal transition to affect embryo implantation by targeting Snai2†.

First Author  Li L Year  2019
Journal  Biol Reprod Volume  100
Issue  5 Pages  1171-1179
PubMed ID  30753312 Mgi Jnum  J:274666
Mgi Id  MGI:6297173 Doi  10.1093/biolre/ioz022
Citation  Li L, et al. (2019) MicroRNA-30a-3p regulates epithelial-mesenchymal transition to affect embryo implantation by targeting Snai2. Biol Reprod 100(5):1171-1179
abstractText  OBJECTIVE: To study the potential role of miR-30a-3p in embryo implantation and explore underlying mechanisms. METHODS: We first established normal pregnancy, pseudopregnancy, delayed implantation, and artificial decidualization mouse models. Next, we detected miR-30a-3p expression profiles of these models with real-time reverse transcription PCR(qRT-PCR), then predicted potential target genes through a dual-luciferase assay. Immunofluorescence-fluorescence in situ hybridization co-located miR-30a-3p and target genes. We then examined the effect of miR-30a-3p on embryo implantation in vivo and in vitro. Wound healing and transwell assays were employed to explore possible miR-30a-3p effects on epithelial-mesenchymal transition (EMT), before molecules related to the latter process were examined with qRT-PCR. RESULTS: MiR-30a-3p expression decreased significantly on embryo implantation day, compared with the peri-implantation period (P < 0.05). Identified target gene Snai2 expression increased significantly during implantation (P < 0.05). In vivo and in vitro analysis showed that up-regulation of miR-30a-3p by agomir and mimics resulted in decreased implantation sites and embryo implantation rate. Transfection of miR-30a-3p mimics to HEC-1-b cells decreased expression of Snai2 and mesenchymal markers (Vimentin and N-cadherin). Furthermore, wound healing area decreased, as did migration and invasion capacity. CONCLUSION: MiR-30a-3p is down-regulated in the embryo implantation period and might have some effect on embryo implantation by acting as a suppressor of EMT through targeting Snai2.
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