Transcription factor TCF7L1 targeting HSPB6 is involved in EMT and PI3K/AKT/mTOR pathways in bladder cancer.

Bladder cancer is notorious for its high recurrence and costly treatment burden, prompting a search for novel therapeutic targets. Our study focuses on HSPB6, a small heat shock protein whose reduced expression in bladder cancer suggests a role in tumor biology. Using an integrative approach of bioinformatics, RNA sequencing, and cell-based assays, we show that HSPB6 upregulation inhibits cancer cell proliferation and metastasis while promoting apoptosis. Moreover, TCF7L1-mediated upregulation of HSPB6 leads to suppression of the PI3K/AKT/mTOR signaling pathway, a key driver of cancer progression. These results position HSPB6 as a compelling target for bladder cancer therapy, and its regulatory role in the PI3K/AKT/mTOR axis underscores its therapeutic potential. Our findings pave the way for future investigations into HSPB6-centered treatment strategies.