ASPM promotes the progression of ovarian endometriosis by modulating the cell cycle and activating the Wnt/β-catenin signaling pathway

<h4>Background</h4>Endometriosis (EMs) is a common gynecological disorder associated with impaired fertility and reduced quality of life. This study investigated abnormal spindle-like microcephaly-associated protein (ASPM), identified as a hub gene in EMs pathogenesis, and explored its functional role and molecular mechanisms.<h4>Materials and methods</h4>Bioinformatics analysis identified key genes associated with EMs. ASPM expression was compared between controls and endometrial tissues or primary endometrial stromal cells from EMs patients. In vitro experiments assessed ASPM's effects on proliferation, invasion, and migration. Transcriptome sequencing revealed ASPM's downstream signaling pathways. Subsequent in vitro experiments demonstrated that ASPM promotes EMs progression via cell cycle regulation and Wnt/β-catenin signaling.<h4>Results</h4>Our bioinformatics analysis identified ASPM as a key differentially expressed hub gene in EMs. Reverse transcription quantitative polymerase chain reaction, immunohistochemistry, and western blot analyses demonstrated elevated ASPM expression in eutopic endometrial tissues and derived primary stromal cells. Functional assays revealed that ASPM knockdown reduced endometrial stromal cell proliferation, invasion, and migration, whereas its overexpression enhanced these cellular processes. Transcriptome sequencing of ASPM-silenced stromal cells implicated cell cycle regulation in ASPM's mechanism of action, with flow cytometry confirming G1 phase arrest following ASPM downregulation. ASPM modulation also altered Wnt/β-catenin signaling pathway activity, with rescue experiments demonstrating that Wnt/β-catenin inhibition counteracted ASPM overexpression effects.<h4>Conclusions</h4>These results suggest ASPM promotes EMs progression via cell cycle regulation and Wnt/β-catenin signaling, offering novel insights into disease pathogenesis.