Open AccessSsc-miR-21-5p regulates endometrial epithelial cells proliferation, apoptosis and migration via the PDCD4/AKT pathway
Author(s) -
Renwu Hua,
Xiuling Zhang,
Wenchao Li,
Weisi Lian,
Qiaorui Liu,
Dengying Gao,
Yueying Wang,
Minggang Lei
Publication year - 2020
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.248898
Subject(s) - biology , protein kinase b , apoptosis , microbiology and biotechnology , cancer research , signal transduction , genetics
Endometrial receptivity plays a vital role in successful embryo implantation in pigs. MicroRNAs (miRNAs), known as the regulator of gene expression, were implicated in the regulation of embryo implantation. However, the role of miRNAs in the endometrial receptivity during the pre-implantation period remains elusive. In this study, we reported that the expression level of ssc-miR-21-5p in porcine endometrium tissues was significantly increased from day 9 to day 12 of pregnancy. Knockdown of ssc-miR-21-5p inhibited proliferation and migration of endometrial epithelial cells (EECs), while induced their apoptosis. We verified that programmed cell death 4 (PDCD4) was a target gene of ssc-miR-21-5p. Inhibition of PDCD4 rescued the effect of ssc-miR-21-5p repression on EECs. Our results also revealed that knockdown of ssc-miR-21-5p impeded the phosphorylation of AKT by targeting PDCD4, which further up-regulated the expression of Bax and down-regulated the levels of Bcl2 and Mmp9. Furthermore, loss of function of mmu-miR-21-5p in vivo resulted in a decreased number of implanted mouse embryos. Taken together, knockdown of ssc-miR-21-5p hampers endometrial receptivity through modulating the PDCD4/AKT pathway.