PMID- 30468451 OWN - NLM STAT- MEDLINE DCOM- 20191119 LR - 20191119 IS - 2284-0729 (Electronic) IS - 1128-3602 (Linking) VI - 22 IP - 21 DP - 2018 Nov TI - LncRNA-TCL6 promotes early abortion and inhibits placenta implantation via the EGFR pathway. PG - 7105-7112 LID - 16242 [pii] LID - 10.26355/eurrev_201811_16242 [doi] AB - 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. FAU - Liu, L-P AU - Liu LP AD - Department of Obstetrics and Gynecology, Hanchuan People's Hospital of Hubei Province, Hanchuan, China. 454586966@qq.com. FAU - Gong, Y-B AU - Gong YB LA - eng PT - Journal Article PL - Italy TA - Eur Rev Med Pharmacol Sci JT - European review for medical and pharmacological sciences JID - 9717360 RN - 0 (RNA, Long Noncoding) RN - 0 (long noncoding RNA TCL6, human) RN - EC 2.7.10.1 (EGFR protein, human) RN - EC 2.7.10.1 (ErbB Receptors) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) SB - IM MH - Abortion, Induced MH - Abortion, Spontaneous/*genetics/metabolism MH - Cell Survival/genetics MH - Embryo Implantation/*genetics MH - ErbB Receptors/metabolism MH - Female MH - Gene Knockdown Techniques MH - Humans MH - Placenta/metabolism MH - Pregnancy MH - Proto-Oncogene Proteins c-akt/metabolism MH - RNA, Long Noncoding/*genetics MH - Signal Transduction MH - Trophoblasts/metabolism EDAT- 2018/11/24 06:00 MHDA- 2019/11/20 06:00 CRDT- 2018/11/24 06:00 PHST- 2018/11/24 06:00 [entrez] PHST- 2018/11/24 06:00 [pubmed] PHST- 2019/11/20 06:00 [medline] AID - 16242 [pii] AID - 10.26355/eurrev_201811_16242 [doi] PST - ppublish SO - Eur Rev Med Pharmacol Sci. 2018 Nov;22(21):7105-7112. doi: 10.26355/eurrev_201811_16242.