Research Paper Volume 13, Issue 11 pp 14924—14939
Nucleolar small molecule RNA SNORA75 promotes endometrial receptivity by regulating the function of miR-146a-3p and ZNF23
- 1 Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, People's Republic of China
- 2 Department of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, People's Republic of China
- 3 Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Zhengzhou 450052, People's Republic of China
Received: November 9, 2020 Accepted: February 9, 2021 Published: May 24, 2021
https://doi.org/10.18632/aging.203007How to Cite
Copyright: © 2021 Wei et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Endometrial receptivity enables the embryo to attach, invade and develop, forming a new individual and species continuity. Small nucleolar RNAs (SnoRNAs) are a class of non-coding RNAs comprising two classes: C/D box snoRNAs and H/ACA box snoRNAs. Aberrant expression of SNORNAs has been reported in tumorigenesis. However, the role of SNORNAs in maintaining endometrial receptivity has not been reported. First, we detected SNORNA expression in endometrial tissues during proliferative and secretory endometrial periods using RNA sequencing. SNORA75 expression was higher in the secretory endometrium, and its overexpression significantly promoted the proliferation, migration and invasion of endometrial cells. The results of analysis with bioinformatics software and RNA pulldown experiments showed that miR-146a-3p interacted with SNORA75. Western blotting showed that miR-146a-3p regulated the expression of ZNF23, whose overexpression significantly promoted the proliferation, migration and invasion of endometrial cells. SNORA75 modulates endometrial receptivity through the miR-146a/ZNF23 signaling pathway.