Abstract
The research endeavors to expound the role of ORM1 in bladder cancer (BCa) and the implied response mechanism. RT-qPCR and Western blotting examined ORM1 and S100A12 expression. Functional experiments assessed the cellular phenotypes. HDOCK and Co-IP confirmed the interaction of ORM1 and S100A12. Western blotting tested apoptosis- and ERK signaling-associated proteins. ORM1 and S100A12 were abundant in the BCa cells. ORM1 or S100A12 loss impaired cell proliferation, migration, and invasion, and aggravated cell apoptosis. ORM1 interacted with S100A12. ORM1 knockdown down-regulated S100A12 expression and inactivated ERK signaling.S100A12 overexpression or ERK activator reversed the impacts of ORM1 interference on ERK signaling and BCa cells. ORM1 mightdrive BCa via binding to S100A12 and activating ERK signaling.