MOXD1 knockdown suppresses the proliferation and tumor growth of glioblastoma cells via ER stress-inducing apoptosis.

Oxygenase-catalyzed reduction and activation of oxygen molecules and the incorporation of oxygen atoms into organic molecules are undoubtedly necessary in the process of tumor development, and it is also one of the research hotspots in recent years. MOXD1 belongs to the copper-dependent monooxygenase family. The expression of MOXD1 is one of the characteristics of early tumor development. However, it is not understandable that the biological function and molecular mechanism of MOXD1 in Glioblastoma (GBM). In this study, high MOXD1 expression is strongly associated with poor survival of the patient with GBM. Moreover. MOXD1 knockdown can inhibit cell viability, proliferation, migration, invasion, and tumorigenesis of GBM cells. This is also proven for the first time that MOXD1 can bind to β3GnT2 and affect the glycosylation modification of some proteins. In addition, knockdown of MOXD1 induces endoplasmic reticulum (ER) stress and triggers the ER-mitochondrial apoptosis pathway. Taken together, these results reveal that MOXD1 is involved in the occurrence and development of GBM, and also provide a new strategy for targeted therapy.