Berberine suppresses bladder cancer cell proliferation by inhibiting JAK1-STAT3 signaling via upregulation of miR-17-5p

Hyperactivation of signal transducer and activator transcription 3 (STAT3) is strongly associated with cancer initiation, progression, metastasis, chemoresistance, immune evasion; thus, STAT3 has been intensely studied as a therapeutic target for treatment. Berberine (BBR), an active component extracted from Coptis chinensis , shown anti-tumor effects in multiple tumors. However, its underlying mechanisms have not yet fully elucidated. In this study, we investigated the BBR on bladder (BCa) cells. We found that showed significant cytotoxic against BCa cell lines both vivo vitro, much lower human normal urothelial line SV-HUC-1. treatment induced DNA replication defects cycle arrest, resulting apoptosis or senescence, depending p53 status, Mechanistically, exerted cells by inhibiting Janus kinase 1 (JAK1)-STAT3 signaling through upregulation miR-17-5p, which directly binds to 3?UTR JAK1 STAT3, downregulating their expressions. Collectively, our results demonstrate exerts perturbing JAK1-STAT3 miR-17-5p cells, may serve potential option