Inhibition of NF-κB activation by BAY 11-7821 suppresses the proliferation and inflammation of glioma cells through inducing autophagy.

Background: Gliomas have been known as the most common intracranial malignant tumor, and this kind of tumors cause huge amounts of mortality. The NF-κB inhibitor BAY 11-7821 has been reported as a novel approach in the immunotherapy of lung diseases. However, the functional role of BAY 11-7821 and its association with autophagy in glioma cells have not yet been reported. Methods: In this study, 2 glioma cell lines (U87 and U251) were treated with different doses of BAY 11-7821, or combined with authphagy inhibitor, 3-MA. Afterwards, Transwell assay, CCK-8 assay, EdU staining, Western blot and immunofluorescence assay was used to detected the cell migration, invasion, vability, autophagy in U87 and U251. Results: Our data showed that BAY 11-7821 significantly suppressed the viability, proliferation, migration, and invasion of glioma cells in a dose-dependent manner. At the molecular level, BAY 11-7821 downregulated the protein levels of p-IκBα, p-p65, NLRP3, and p62, and upregulated the protein levels of caspase 3 and Bax, as well as decreased the levels of IL-1β and IL-18. Results showed BAY 11-7821 enhanced autophagy. While, Pre-treatment with 3-MA, an autophagy inhibitor, obviously reversed the effects of BAY 11-7821 on malignant biological behaviors of glioma cell, inflammation status, and autophagy. Conclusions: In this study, we found that BAY 11-7821 has an effective inhibitive function on malignant biological behaviors by mediating autophagy. Our findings contribute to a better understanding of BAY 11-7821 as a potential anticancer drug in glioma via activating autophagy.