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The following is a summary of “Cytokeratin 17 activates AKT signaling to induce epithelial-mesenchymal transition and promote bladder cancer progression,” published in the April 2025 issue of BMC Urology by Zhang et al. 

Bladder cancer is a common and aggressive tumor of the urinary tract. Identifying key molecular targets is crucial for improving prognosis and treatment. 

Researchers conducted a retrospective study to explore how cytokeratin 17 promotes bladder cancer progression by inducing epithelial-mesenchymal transition (EMT) via AKT activation. 

They collected 78 bladder cancer tissue specimens, detected cytokeratin 17 (CK17) expression in cancer and paracancerous tissues via immunohistochemistry, and analyzed its link to prognosis through follow-up. Western Blot assessed CK17 levels in bladder cancer cell lines, and CK17-silenced and overexpressed lines were constructed using T24 (high CK17) and 5637 (low CK17) cells. Flow cytometry, Cell Counting Kit-8 (CCK-8), Trans-well, and scratch assays evaluated proliferation, migration, and invasion. Western Blot and immunofluorescence detected EMT markers, and AKT Ser473 and Thr308 phosphorylation levels were measured by Western Blot. 

The results showed CK17 was significantly upregulated in cancer tissues compared to paracancerous tissues, and high CK17 levels indicated shorter progression-free survival and poorer prognosis. CK17 expression correlated with tumor grade and TNM stage. Overexpression in 5,637 cells promoted proliferation, migration, and invasion, while silencing in T24 cells inhibited these functions. CK17 overexpression increased AKT (Ser473) phosphorylation and upregulated vimentin, N-cadherin, Slug, and Twist; silencing CK17 showed opposite effects. 

Investigators found that high CK17 expression promoted proliferation, migration, invasion, and EMT through AKT-Ser473 phosphorylation. They concluded that CK17 was associated with malignant progression and poor prognosis, suggesting its potential as a therapeutic target. 

Source: bmcurol.biomedcentral.com/articles/10.1186/s12894-025-01760-4