circFAM120A participates in repeated implantation failure by regulating decidualization via the miR‐29/ABHD5 axis

基因敲除 蜕膜化 荧光素酶 细胞生物学 间质细胞 子宫内膜 生物 分子生物学 男科 基因 转染 医学 癌症研究 内分泌学 遗传学
作者
Tingting Zhou,Tianxiang Ni,Yan Li,Qian Zhang,Junhao Yan,Zi‐Jiang Chen
出处
期刊:The FASEB Journal [Wiley]
卷期号:35 (9) 被引量:9
标识
DOI:10.1096/fj.202002298rr
摘要

Abstract Repeated implantation failure (RIF) is a major problem that limits the pregnancy rate associated with assisted reproductive technology. However, the pathogenesis of RIF is still unknown. Recently, the expression levels of circular RNAs (circRNAs) were profiled in the endometrial tissues of patients with RIF. However, the exact role of circRNAs in RIF remains unclear. In our study, we found that circFAM120A levels were significantly down‐regulated in the endometrium at the window of implantation in RIF patients compared with non‐RIF controls. The suppression of circFAM120A expression inhibited decidualization in human endometrial stromal cells (hESCs). Furthermore, RNA‐seq analysis after circFAM120A knockdown revealed ABHD5 as a potential downstream target gene of circFAM120A . As expected, down‐regulating ABHD5 in hESCs also inhibited decidualization. Using the starBase and TargetScan databases, we predicted that miR‐29 may interact with ABHD5 , based on nucleotide sequence matching. Luciferase reporter assay showed that miR‐29 bound to the 3′ UTR of ABHD5 at the predicted complementary sites. Moreover, miR‐29 mimics efficiently reduced ABHD5 expression levels and suppressed the decidualization process, whereas a miR‐29 inhibitor partly rescued ABHD5 mRNA expression level and decidualization reduced by the knockdown of circFAM120A . Therefore, circFAM120A modulated decidualization in RIF through the miR‐29 / ABHD5 axis.
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