Flow cytometry revealed no significant changes in CD44 expression but showed a moderate increase in CD133+ cells following ESRP2 overexpression, suggesting a qualitative shift in stem-like subpopulations rather than a global suppression of cancer stemness.<h4>Discussion</h4>These findings identify ESRP2 as a key post-transcriptional regulator that constrains EMT-associated transcriptional programs linked to ZEB1 expression, thereby stabilizing epithelial identity in bladder cancer. Here, PROM1 is linked to urinary bladder carcinoma.