Gliomas are the most common malignant brain tumor in the central nervous system. They are characterized by high invasiveness and heterogeneity. In recent years, cancer-derived immunoglobulin G (Cancer-IgG) has received significant attention from researchers. Cancer-IgG, identified from tumors, can promote tumorigenesis and tumor progression. In this study, we explored the expression patterns of Cancer-IgG using available datasets and validated these patterns in our patient samples. Several loss-of-function and gain-of function assays were performed to investigate the roles of Cancer-IgG. Potential mechanisms underlying these roles were investigated using co-immunoprecipitation and RNA sequencing. Our result demonstrated that Cancer-IgG is expressed in gliomas. Furthermore, the expression of Cancer-IgG is associated with a poor prognosis and malignant molecular characterization. Functional assays confirmed that Cancer-IgG can promote glioma cells proliferation, migration, invasion, and resistant to apoptosis. The cGMP/PKG/VASP pathway is potentially involved in the effects of Cancer-IgG. Evidence from co-culture assay suggest that Cancer-IgG can induce M2 polarization of macrophages. In conclusion, Cancer-IgG can be identified in glioma cells and promotes the development of a malignant biological phenotype in vivo and in vitro. In glioma microenvironment, Cancer-IgG can induce M2 polarization of macrophages.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.intimp.2024.113314 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!