Premium
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
Author(s) -
Liu Xiaorui,
Zhang Lei,
Yang Lichun,
Cui Jiuzeng,
Che Sicheng,
Liu Yuexia,
Han Jincheng,
An Xiaopeng,
Cao Binyun,
Song Yuxuan
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29821
Subject(s) - pi3k/akt/mtor pathway , mapk/erk pathway , protein kinase b , apoptosis , cancer research , microbiology and biotechnology , microrna , chemistry , signal transduction , biology , gene , biochemistry
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.