Liu Zhe, Pu Xiaofeng
Department of Urology, Wuxi No. 2 People's Hospital (Jiangnan University Medical Center), Wuxi, China.
Department of Urology, Chongqing General Hospital, Chongqing University, Chongqing, China.
Cell Adh Migr. 2025 Dec;19(1):1-11. doi: 10.1080/19336918.2024.2434209. Epub 2024 Dec 7.
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.
该研究旨在阐述ORM1在膀胱癌(BCa)中的作用及潜在的反应机制。采用RT-qPCR和蛋白质免疫印迹法检测ORM1和S100A12的表达。通过功能实验评估细胞表型。利用HDOCK和免疫共沉淀法证实ORM1与S100A12的相互作用。蛋白质免疫印迹法检测凋亡相关蛋白和ERK信号通路相关蛋白。ORM1和S100A12在膀胱癌细胞中表达丰富。敲低ORM1或S100A12会损害细胞增殖、迁移和侵袭能力,并加剧细胞凋亡。ORM1与S100A12相互作用。敲低ORM1会下调S100A12的表达并使ERK信号通路失活。过表达S100A12或使用ERK激活剂可逆转ORM1干扰对ERK信号通路和膀胱癌细胞的影响。ORM1可能通过与S100A12结合并激活ERK信号通路来驱动膀胱癌的发生发展。