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PRMT1 drives cervical cancer progression by orchestrating cell growth, migration, and angiogenesis
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DOI：10.1093/hmg/ddag044.png)
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Abstract
En 中文
PRMT1 is an important regulator implicated in multiple malignancies, yet its role in cervical cancer remains unclear. In this study, we investigated the functional significance of PRMT1 in cervical cancer using integrated public transcriptomic datasets, CRISPR/Cas9-edited HeLa cells, and an in vivo xenograft model. PRMT1 was upregulated in cervical cancer tissues and was associated with histological grade, clinical stage, and lymph node metastasis status, although it was not significantly associated with overall survival. In vitro, PRMT1 depletion inhibited cell proliferation, colony formation, aggregation, and migration, and was accompanied by mitochondrial apoptosis, S-phase arrest, altered c-Myc and PI3K/AKT signaling, and changes in EMT-related marker expression. Conditioned medium from PRMT1-knockout cells also impaired human umbilical vein endothelial cells (HUVECs) tube formation and was associated with reduced MMP-9 expression. In vivo, PRMT1 knockout significantly suppressed xenograft growth and reduced Ki-67 and CD31 expression. Collectively, these findings suggest that PRMT1 is an important regulator associated with cervical cancer progression and a potential candidate biomarker for prognostic assessment and therapeutic targeting, although its clinical prognostic value requires further validation.
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