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

Xin Liu, Rongyan Qin, Fengque Zheng
Medicine · 2026 · vol. 105(20) , pp. e48765 · doi:10.1097/md.0000000000048765 · PMID:42152408 · PMC13183157 · W7161240535
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

ASPM promotes ovarian endometriosis by regulating the cell cycle and activating the Wnt/β-catenin signaling pathway, as demonstrated by increased ASPM expression and functional assays in endometrial stromal cells.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-12 ⓘ

The paper investigated the role of abnormal spindle-like microcephaly-associated protein (ASPM) in endometriosis by integrating four endometrial mRNA microarray datasets to identify differentially expressed genes, building a protein-protein interaction network, and highlighting hub genes for pathway enrichment, followed by experimental testing in endometrial stromal cells (ESCs). It reported that ASPM was dysregulated and that ASPM promotes ESC proliferation, invasion, and migration while modulating the cell cycle and activating Wnt/β-catenin signaling, including changes in Cyclin D1 and c‑Myc alongside β-catenin. The main limitation is that experimental ESCs were isolated from a small number of patients (6 with endometriosis and 8 controls) due to tissue availability, and the manuscript provides limited detail on downstream functional validation of key bioinformatics-identified hub genes beyond ASPM perturbation. This paper is centrally about endometriosis — specifically ovarian endometriosis and its promotion of progression through ASPM-dependent cell cycle regulation and Wnt/β-catenin pathway activation in ESCs.

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Abstract

BACKGROUND: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: These results suggest ASPM promotes EMs progression via cell cycle regulation and Wnt/β-catenin signaling, offering novel insights into disease pathogenesis.

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Condition tags

endometriosis

MeSH descriptors

Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Cell Cycle Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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