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• W2408413844 abstract "Embryo implantation is regarded as a critical physiological process for the success of pregnancy. There are so many reports on the research of human chorionic gonadotropin (HCG) in artificial insemination, but the impact of HCG on endometrial receptivity has not been elucidated. Beta1, 4-Galactosyltransferase-I (β1,4-GalT-I) is ubiquitously expresses in human tissues with the exception of the brain. It not only transfers galactose from UDP-galactoside to GlcNAc to form Galβl,4-GlcNAc, but plays crucial role as cell adhesion molecule by recognizing and adhering other extracellular matrix and galactose of cell surface glycoprotein and glycolipid in cancer cells invasion and migration. The process of the embryos implantation is very similar to tumor invasion, so many biological factors participate in the tumor invasion also play a role in embryo implantation. We hypothesize that β1,4-GalT-I may take part in embryo implantation. In this study, we demonstrated that the over expression of β1,4-GalT-I was induced by HCG in RL95-2 cells. Moreover, the expression of some molecules, such as TIMP-1, LN and MMPs could be regulated by engineered expression of β1,4-GalT-I and therefore lead to the significantly alteration of adhesion capability of RL95-2 cells, even result in reduced adhesive ability between JAR cells and RL95-2 cells. Furthermore, our results indicated that HCG can obviously increase the EGFR signaling pathways-dependent molecular expression through β1,4-GalT-I, HCG also improved the adhesive ability between JAR cells and RL95-2 cells (P<0.01). Taken together, our data suggested that HCG provides a mechanism to bridge embryo to endometrium through β1,4-GalT." @default.
• W2408413844 created "2016-06-24" @default.
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• W2408413844 date "2015-01-01" @default.
• W2408413844 modified "2023-09-23" @default.
• W2408413844 title "HCG induces β1,4-GalT I expression and promotes embryo implantation." @default.
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• W2408413844 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4503029" @default.
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