Unveiling Oncogenic Power of WAVE1 in Bladder Cancer Progression

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Shouxi Cui¹, Bin Liang¹, Yong Liu^2,a*

¹Department of Urology, Changzhou Cancer Hospital, Changzhou, 213000, China

²Department of Oncology, Changzhou Cancer Hospital, Changzhou, 213000, China

^* To whom correspondence should be addressed.

Received: December 10, 2024; Revised: March 27, 2025; Accepted: April 22, 2025

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WAVE1 (Wiskott–Aldrich syndrome verprolin-homologous protein family member 1), a gene associated with the Wiskott–Aldrich syndrome, has been identified as an oncogene with high expression in various tumors and has been linked to metastatic conditions. Nevertheless, expression pattern of WAVE1 and its function in bladder cancer (BC) remain unknown. This study aimed to uncover the effect of WAVE1 on migration and metastasis in BC. In this study, four different human urinary BC cell lines (T24, RT4, J82, and BIU87) were examined using immunohistochemical and Western blot assays to assess the pattern of WAVE1 expression. Subsequently, the regulatory role of WAVE1 expression in migration, and EMT in the BC cell lines was investigated. WAVE1 was significantly expressed in the BC tissues in vivo. WAVE1 knockdown in the T24 cells inhibited cell migration, whereas WAVE1 upregulation in the RT4 cells had the opposite effect. WAVE1 was shown to trigger epithelial-mesenchymal transition (EMT) and stimulate the p38 mitogen-activated protein kinase (MAPK) signaling pathway. The findings indicate that WAVE1 enhances migration and invasion of the BC cells through EMT, which is mediated by activation of the MAPK/p38 signaling.

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KEY WORDS: bladder cancer, Wiskott–Aldrich syndrome verprolin-homologous 1, WAVE1, oncogene, migration and metastasis, epithelial to mesenchymal transition

DOI: 10.1134/S0006297924604489

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