LncRNA-TCL6 通过 EGFR 通路促进早期流产和抑制胎盘植入。
LncRNA-TCL6 promotes early abortion and inhibits placenta implantation via the EGFR pathway.
机构信息
Department of Obstetrics and Gynecology, Hanchuan People's Hospital of Hubei Province, Hanchuan, China.
出版信息
Eur Rev Med Pharmacol Sci. 2018 Nov;22(21):7105-7112. doi: 10.26355/eurrev_201811_16242.
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.
目的
本研究旨在探讨长链非编码 RNA（lncRNA）TCL6 在早期流产中的作用，并探讨其潜在机制。
患者与方法
采用实时定量聚合酶链反应（qRT-PCR）分别检测正常妊娠、先兆流产妊娠、自然流产妊娠和人工流产妊娠胎盘组织中 lncRNA-TCL6 和表皮生长因子受体（EGFR）的表达水平。用 siRNA 转染滋养细胞以敲低 lncRNA-TCL6。用细胞计数试剂盒-8（CCK-8）法检测滋养细胞的活力。用 Western blot 检测 lncRNA-TCL6 敲低后滋养细胞中 EGFR、细胞外调节蛋白激酶（ERK）和蛋白激酶 B（AKT）的蛋白表达水平。进行挽救实验以研究 EGFR 与 lncRNA-TCL6 之间的关系。
结果
先兆流产妊娠胎盘组织中 lncRNA-TCL6 的表达明显高于正常妊娠。同时，自然流产妊娠胎盘组织中 lncRNA-TCL6 的表达也明显高于人工流产妊娠。然而，EGFR 的表达则呈现相反的趋势。在滋养细胞中敲低 lncRNA-TCL6 后，与对照组相比，EGFR、ERK 和 AKT 的蛋白表达水平显著增加。CCK-8 检测表明，敲低 lncRNA-TCL6 后细胞活力明显增加，而 EGFR 敲低则可逆转这一现象。
结论
与正常妊娠相比，先兆流产妊娠胎盘组织中 lncRNA-TCL6 表达水平升高。此外，自然流产妊娠胎盘组织中 lncRNA-TCL6 的表达明显高于人工流产妊娠。敲低 lncRNA-TCL6 通过 EGFR 信号通路促进滋养细胞的增殖并抑制流产。
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