Aberrant WDR5 promotes the progression of cervical cancer through the YAP1- CTGF pathway
WDR5 plays a pivotal role in promoting cancer progression across various malignancies. However, its involvement in cervical cancer remains poorly understood. This study aims to elucidate the mechanisms by which WDR5 drives cervical cancer progression. Cervical cancer tissues were analyzed to assess WDR5 regulation. In vitro assays evaluated the effects of WDR5 loss-of-function on cell proliferation, migration, and invasion. Mechanistic studies investigated the interaction between WDR5 and YAP1, and the subsequent modulation of CTGF gene expression via histone 3 lysine 4 trimethylation. Xenograft tumor models were utilized to examine the in vivo role of WDR5 in cervical cancer progression. WDR5 is significantly upregulated in cervical cancer tissues and correlates with poor prognosis. Loss of WDR5 function markedly suppresses cervical cancer cell proliferation, migration, and invasion in vitro. WDR5 interacts with YAP1, enhancing CTGF expression through histone methylation. In vivo, the oncogenic function of WDR5 is contingent upon the YAP1-CTGF signaling axis. This study identifies the WDR5/YAP1/CTGF pathway as a key mechanism in cervical cancer progression, suggesting that targeting this axis may provide a promising therapeutic approach.