AIF-1 Modulates Endometrial Stromal Cell Proliferation, Invasion, and Migration via Mitochondrial Function

Abstract

This study investigates the role of allograft inflammatory factor 1 (AIF-1) in regulating the proliferation, invasion, and migration of endometrial stromal cells (ESCs) in the context of endometriosis, focusing on its impact on mitochondrial function. Ectopic endometrial tissues were collected from patients diagnosed with endometriosis, and normal endometrial tissues served as controls. ESCs were isolated and cultured. AIF-1 expression was knocked down using siRNA and overexpressed using plasmid vectors. Quantitative real-time PCR (qRT-PCR), western blot analysis, CCK-8 assays, flow cytometry, transwell assays, scratch assays, ATP detection, and mitochondrial membrane potential assays were performed to evaluate gene expression, cell proliferation, apoptosis, invasion, and mitochondrial function. AIF-1 mRNA and protein levels were significantly upregulated in ectopic ESCs compared to controls. Overexpressing AIF-1 elevated cell proliferation and invasion and decreased apoptosis. Additionally, AIF-1 knockdown decreased mitochondrial DNA copy number, membrane potential, and ATP levels, whereas its overexpression had the opposite effects. AIF-1 plays a crucial role in ESCs proliferation, invasion, and migration by modulating mitochondrial function, potentially via the AIF-1 pathway. These findings suggest that targeting AIF-1 could be a novel therapeutic approach for managing endometriosis.