ERO1A promotes the proliferation, migration and invasion of bladder cancer through ALOX5 mediated activation of JAK-STAT signaling pathway.

BACKGROUND: Endoplasmic reticulum oxidoreductase 1 A (ERO1A) is a protein disulfide oxidoreductase. ERO1A is involved in the progression of various tumors, but the potential mechanism of its action in bladder cancer remains unclear. METHODS: In this study, we utilized data from public databases to investigate the expression pattern of ERO1A. Through CCK-8, EdU, wound healing, and Transwell invasion assays, we evaluated the effects of ERO1A on the proliferation, migration, and invasion abilities of bladder cancer cells. We further explored the specific molecular mechanism of ERO1A. Finally, a subcutaneous tumor formation model in nude mice was established to detect the function of ERO1A in vivo. RESULTS: Silencing the expression of ERO1A inhibits the proliferation, migration and invasion of bladder cancer cells, and also suppresses tumor growth in vivo. Mechanistically, ERO1A binds to and suppresses the phosphorylation of ALOX5, which in turn activates the JAK-STAT signaling pathway and subsequently suppresses autophagy. CONCLUSION: In conclusion, this study demonstrates that ERO1A could promote the proliferation, migration, and invasion of bladder cancer cells by regulating the ALOX5/JAK/STAT/autophagy signaling axis. ERO1A may serve as a novel molecular marker for the diagnosis and treatment of clinical bladder cancer patients.