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Objective: Impaired endometrial receptivity is the main cause of embryo implantation failure. Little information is available on the role of circRNAs in endometrial receptivity. Here, the effect of circABCC1 on endometrial receptivity and its mechanism were investigated.
Methods: GEO database was screened for key biomarkers for recurrent implantation failure (RIF). Endometrial epithelial cells (EECs) were cultured and transfected with circABCC1- and/or FAM155B-related vectors, followed by CCK-8 detection of cell proliferation, western blotting detection of receptivity-related factors LIF and DKK1, and ELISA detection of LIF secretion. An adhesion model was established to detect trophoblast adhesion to EECs. RIP was used to detect the binding of METTL3 to circABCC1 and FAM155B mRNA, and MeRIP-qPCR was used to detect mA modification of FAM155B mRNA.
Results: CircABCC1 and FAM155B were highly expressed in patients with RIF. CircABCC1 or FAM155B overexpression reduced EEC proliferation, LIF and DKK1 expression, LIF secretion, and trophoblast adhesion; circABCC1 or FAM155B knockdown led to the opposite results. CircABCC1 and METTL3 positively regulated FAM155B expression. METTL3 bound circABCC1 and FAM155B mRNA. METTL3 overexpression increased mA modification of FAM155B mRNA. FAM155B overexpression partially eliminated circABCC1 knockdown-induced promotion of EEC proliferation, LIF and DKK1 expression, LIF secretion, and trophoblast adhesion.
Conclusion: CircABCC1 binds to METTL3 to regulate FAM155B mRNA modification and promote FAM155B expression, thereby inhibiting EEC proliferation and reducing endometrial receptivity.
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http://dx.doi.org/10.1080/14767058.2024.2416603 | DOI Listing |
FASEB J
September 2025
Department of Obstetrics, Gynecology and Women's Health, University of Missouri School of Medicine, Columbia, Missouri, USA.
Ovarian steroid hormones-estrogen and progesterone-play a central role in regulating epithelial-stromal interactions in the uterus. These interactions are critical for uterine function, including endometrial receptivity, implantation, and decidualization. These interactions involve complex signaling crosstalk between the uterine epithelium and the underlying stroma, with dynamic cell population-specific roles.
View Article and Find Full Text PDFGeorgian Med News
June 2025
6Municipal State Enterprise "City Center for Human Reproduction" under the Public Health Department, Almaty, Kazakhstan.
Introduction: Antiphospholipid syndrome is an autoimmune disease marked by antiphospholipid antibodies, causing thrombosis and obstetric complications.
Objectives: This study explores molecular mechanisms, endometrial receptivity, and clinical parameters linked to APS, focusing on pregnancy complications such as miscarriage, preterm delivery, recurrent implantation failure (RIF), and thrombosis.
Patients And Methods: A systematic review was conducted through Scopus, WoS, PubMed, Cochrane, and Google Scholar, including studies published between 2019 and 2024.
J Clin Med
August 2025
ART Center of the Department of Obstetrics and Gynecology, CHU of Liège-Citadelle Site, University of Liège, 4000 Liege, Belgium.
: The management of patients with recurrent implantation failure (RIF) or recurrent pregnancy loss (RPL) is a real challenge. Studying endometrial proliferation and vascularization by ultrasound during the embryo implantation window is an option for investigating these failures. This approach involves measuring the endometrial volume, the uterine arteries pulsatility index (PI), and the sub-endometrial flow index (VFI).
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Department of Reproductive Medecine, Aziza Othmana University-Hospital, Health Ministry, Tunis 1008, Tunisia.
Endometriosis, a chronic estrogen-dependent disorder defined by ectopic endometrial-like tissue growth, causes pelvic pain and infertility in reproductive-age women. Despite its prevalence, the underlying mechanisms driving lesion persistence and reproductive impairment remain unclear. This review synthesizes recent pathophysiological advances, highlighting how hormonal dysregulation, immune dysfunction, epigenetic alterations, and oxidative stress collectively foster lesion persistence and treatment resistance.
View Article and Find Full Text PDFBiomedicines
August 2025
Department of Public Health, School of Medicine, University of Naples "Federico II", 80131 Naples, Italy.
Polycystic ovary syndrome (PCOS) is a complex and multifactorial disorder affecting reproductive, endocrine, and metabolic functions in women of reproductive age. While environmental and lifestyle factors play a role, increasing evidence highlights the contribution of genetic and epigenetic mechanisms to its pathogenesis. This narrative review aims to provide an updated overview of the current evidence regarding the role of genetic variants, gene expression patterns, and epigenetic modifications in the etiopathogenesis of PCOS, with a focus on their impact on ovarian function, fertility, and systemic alterations.
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