Repression of Septin9 inhibits the oncogenic phenotype of bladder cancer

Septin 9 (SEPT9) is a member of the GTPase family and has a vital role in metastasis due to its role in cytoskeletal structure, actin remodeling process, and cell migration. Although SEPT9 has been implicated in the pathogenesis of several cancers, its role in bladder cancer remains unclear.

SEPT9 expression in bladder cancer tissues was analyzed using at both transcriptional and translational levels and also validated in clinical specimens using Gene Expression Omnibus (GEO) datasets. Additionally, the SEPT9 promoter methylation level was determined by bioinformatics analysis. Following SEPT9 suppression, cell proliferation and migration were examined using colony formation, transwell and wound-healing assays. QRT-PCR and western blotting also evaluated epithelial-mesenchymal transition (EMT) markers.

Analysis of GEO datasets and clinical samples revealed high SEPT9 expression in bladder cancer tissues. Hypermethylation of the SEPT9 promoter did not affect expression levels. SEPT9 suppression significantly reduced cell proliferation, invasion and migration. Furthermore, SEPT9 suppression decreased N-cadherin and vimentin expression while increasing E-cadherin expression, suggesting a possible role in EMT.

In this study, SEPT9 overexpression was shown to contribute to the oncogenic phenotype of bladder cancer and could serve as a potential early-stage biomarker. Moreover, SEPT9 may offer new avenues for developing more effective targeted therapeutic approaches for bladder cancer. Future studies addressing this aspect will be important for better defining the role of SEPT9 across diverse bladder cancer contexts.