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CDC20 inhibitor Apcin inhibits embryo implantation in vivo and in vitro. Guo Chuanjia,Kong Fandou,Lv Yunyi,Gao Na,Xiu Xiaoxin,Sun Xiaojing Cell biochemistry and function For successful implantation, endometrial receptivity must be established. The high expression of CDC20 in many kinds of malignant tumours has been reported, and it is related to the occurrence and development of tumours. According to these functions, we think that CDC20 may also play important roles in the process of embryo implantation. To prove our hypothesis, we observed the distribution and expression of CDC20 in mouse and human early pregnancy. The effect of E2 and/or P4 on the expression of CDC20 in human endometrial cells was detected by Western blot. To further explore whether CDC20 is an important factor in adhesion and proliferation. The results showed that the expression of CDC20 in the uterus and menstrual cycle of early pregnant mice was spatiotemporal. E2 can promote the expression of CDC20. On the contrary, P4 and E2 + P4 inhibited the expression of CDC20. We also detected the proliferation and adhesion of human endometrial cells. We found that the inhibition of CDC20 with its inhibitor Apcin could reduce the adhesion rate and proliferation ability to RL95-2 and HEC-1A cells, respectively. Inhibiting CDC20 by Apcin could interfere the embryo implantation of mouse. It is suggested that CDC20 may play an important role in the process of embryo implantation. SIGNIFICANCE OF THE STUDY: Embryo implantation is an extremely complex and delicate process, including identification, localisation, adhesion and invasion between embryo and endometrium. Studies have shown the process of embryo implantation is very similar to that of tumour invasion. CDC20 is a cancer-promoting factor. We found CDC20 is spatially and spatially expressed in mouse and human menstrual cycles and is regulated by oestrogen and progesterone. Apcin can inhibit the adhesion of JAR cells and embryo implantation of mouse. CDC20 may provide a new way to improve the success rate of assisted reproduction. 10.1002/cbf.3550
LncRNA-TCL6 promotes early abortion and inhibits placenta implantation via the EGFR pathway. Liu L-P,Gong Y-B European review for medical and pharmacological sciences OBJECTIVE:The aim of this study was to investigate the role of long non-coding RNA (lncRNA) TCL6 in early abortion and to explore its underlying mechanism. PATIENTS AND METHODS:The expression levels of lncRNA-TCL6 and epidermal growth factor receptor (EGFR) in placental tissues of normal pregnancy, threatened abortion pregnancy, spontaneous abortion pregnancy, and induced abortion pregnancy were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), respectively. Trophoblast cells were transfected with siRNA to knock-down lncRNA-TCL6. Cell viability of trophoblast cells was detected by cell counting kit-8 (CCK-8) assay. The protein expression levels of EGFR, extracellular regulated protein kinases (ERK) and protein kinase B (AKT) in trophoblast cells after lncRNA-TCL6 knockdown were detected by Western blot. Rescue experiments were performed to investigate the relationship between EGFR and lncRNA-TCL6. RESULTS:The expression of lncRNA-TCL6 in placenta tissues of threatened abortion pregnancy was significantly higher than that of normal pregnancy. Meanwhile, the expression of lncRNA-TCL6 in placenta tissues of spontaneous abortion pregnancy was also markedly higher than induced abortion pregnancy. However, the expression of EGFR showed an opposite trend. After knockdown of lncRNA-TCL6 in trophoblast cells, the protein expression levels of EGFR, ERK, and AKT were significantly increased when compared with those of the control group. CCK-8 assay indicated that cell viability was remarkably increased after knockdown of lncRNA-TCL6, which could be reversed by EGFR knockdown. CONCLUSIONS:Compared with normal pregnancy, lncRNA-TCL6 was highly expressed in placental tissues of threatened abortion pregnancy. Moreover, the expression of lncRNA-TCL6 in placenta tissues of spontaneous abortion pregnancy was significantly higher than induced abortion pregnancy. Knockdown of lncRNA-TCL6 promoted the proliferation of trophoblast cells and inhibited the abortion via the EGFR signaling pathway. 10.26355/eurrev_201811_16242