Treating T24 cells with erianin restores gefitinib drug sensitivity by regulating MYLK to inhibit EGFR and EMT processes.

Erianin exerts anticancer effects in bladder cancer, although its underlying molecular mechanisms remain unclear. This study used online databases to identify erianin-related drug targets and bladder cancer-associated disease targets and to predict the potential signaling pathways involved. Intersecting genes were enriched in the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance signaling pathway, and high myosin light chain kinase (MYLK) expression was associated with poor prognosis. A gefitinib-resistant bladder cancer cell line was established to evaluate the role of MYLK. Erianin inhibited MYLK and EGFR protein expression, blocked EGFR signaling and epithelial-mesenchymal transition (EMT), restored gefitinib sensitivity, and suppressed the proliferation, invasion, and migration of bladder cancer cells.