miR-34a/c induce caprine endometrial epithelial cell apoptosis by regulating circ-8073/CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways.,Journal of Cellular Physiology

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miR-34a/c induce caprine endometrial epithelial cell apoptosis by regulating circ-8073/CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways.
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-05-31 , DOI: 10.1002/jcp.29821
Xiaorui Liu ₁ , Lei Zhang ₁ , Lichun Yang ₁ , Jiuzeng Cui ₁ , Sicheng Che ₁ , Yuexia Liu ₁ , Jincheng Han ₁ , Xiaopeng An ₁ , Binyun Cao ₁ , Yuxuan Song ₁

Affiliation

microRNAs (miRNAs) and circular RNAs (circRNAs) are important for endometrial receptivity establishment and embryo implantation in mammals. miR‐34a and miR‐34c are highly expressed in caprine receptive endometrium (RE). Herein, the functions and mechanisms of miR‐34a/c in caprine endometrial epithelial cell (CEEC) apoptosis and RE establishment were investigated. miR‐34a/c downregulated the expression level of centrosomal protein 55 (CEP55) and were sponged by circRNA8073 (circ‐8073), thereby exhibiting a negative interaction in CEEC. miR‐34a/c induced CEEC apoptosis by targeting circ‐8073/CEP55 through the regulation of the RAS/RAF/MEK/ERK and phosphoitide 3‐kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathways. Positive and negative feedback loops and cross‐talk were documented between the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways. miR‐34a/c regulated the levels of RE marker genes, including forkhead box M1, vascular endothelial growth factor, and osteopontin (OPN). These results suggest that miR‐34a/c not only induce CEEC apoptosis by binding to circ‐8073 and CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways, but may also regulate RE establishment in dairy goats.

中文翻译：

miR-34a / c通过RAS / RAF / MEK / ERK和PI3K / AKT / mTOR途径调节circ-8073 / CEP55诱导山羊子宫内膜上皮细胞凋亡。

microRNA（miRNA）和环形RNA（circRNA）对于哺乳动物的子宫内膜容受性建立和胚胎植入非常重要。miR-34a和miR-34c在山羊接受性子宫内膜（RE）中高表达。本文研究了miR-34a / c在小鼠子宫内膜上皮细胞（CEEC）凋亡和RE建立中的功能和机制。miR-34a / c下调了中心体蛋白55（CEP55）并用circRNA8073（circ-8073）擦拭，从而在CEEC中表现出负向相互作用。miR-34a / c通过调节RAS / RAF / MEK / ERK和磷酸3激酶（PI3K）/蛋白激酶B（AKT）/雷帕霉素哺乳动物靶点（mTOR）靶向circ-8073 / CEP55诱导CEEC凋亡途径。RAS / RAF / MEK / ERK和PI3K / AKT / mTOR通路之间记录了正反馈回路和负反馈回路以及串扰。miR-34a / c调节RE标记基因的水平，包括叉头盒M1，血管内皮生长因子和骨桥蛋白（OPN）。这些结果表明，miR-34a / c不仅通过RAS / RAF / MEK / ERK和PI3K / AKT / mTOR途径与circ8073和CEP55结合，从而诱导CEEC凋亡，而且还可能调节乳山羊的RE形成。

更新日期：2020-05-31

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