Emerging strategies and translational advancements of DDR1 in oncology.

Discoidin domain receptor 1 (DDR1) has emerged as a promising therapeutic target in oncology due to its unique role in tumor-stroma interactions and its involvement in key signaling pathways that drive cancer progression. DDR1 is homologous to the transmembrane receptor tyrosine kinase (RTK) family and uniquely requires binding to collagen for its activation. It regulates several cellular processes related to tumor cell proliferation, metabolism, migration, stromal remodeling, and epithelial-mesenchymal transition (EMT), ultimately influencing patient survival. Dysregulation of DDR1 may contribute to cancer progression, neurodegenerative diseases, fibrotic conditions, and atherosclerosis. Moreover, DDR1 has been shown to affect a wide variety of cancers, including lung, breast, stomach, colon, ovarian, and pancreatic cancers, underscoring its potential as a therapeutic target. Various small-molecule tyrosine kinase inhibitors aimed at DDR1 have been developed and have demonstrated significant effectiveness in reducing tumor growth. This review focuses on the structure, function, and mechanism of DDR1, as well as its involvement in cancer progression. Additionally, it examines the development and therapeutic potential of DDR1 inhibitors, offering a comprehensive overview of their application in cancer treatment. By synthesizing current knowledge, this article provides valuable insights to guide future research and innovation in targeting DDR1 for clinical therapeutic advancement.