CCT5 as a candidate biomarker in bladder cancer: functional validation and mechanistic clues

using xenografts. To elucidate the underlying mechanisms, RNA-seq was integrated with Western blotting analysis. CCT5 was found to be upregulated in bladder cancer and correlated with poor prognosis and aggressive pathological features. Single-cell and spatial analyses revealed that CCT5 was enriched in malignant epithelial subpopulations with high CNV scores, activated oncogenic pathways, and extensive cell-cell interactions. Functionally, CCT5 promoted proliferation, migration, invasion, and G1/S transition while inhibiting apoptosis; its depletion reduced xenograft growth. At the signaling level, CCT5 knockdown enhanced phosphorylation of MST1, LATS1, and YAP, without significant changes in total protein levels, suggesting activation of Hippo/YAP signaling. These findings highlight CCT5 as an oncogenic factor in bladder cancer, potentially acting through the regulation of Hippo/YAP signaling, and propose its potential as a biomarker and therapeutic target in bladder cancer.