Fig. 6: Targeting the MDK signaling pathway in GBM can affect intracranial tumor growth and immune microenvironment.

A A mouse GBM intracranial implantation model was established by implanting stable overexpression of MDK molecule GL261 cell lines into the right striatum of mice, divided into MDK_NC, MDK_OE, and MDK_OE+iMDK (n = 10) according to different treatment methods. B, C In vivo imaging technology was used to monitor intracranial tumor growth every week, and the Kaplan–Meier survival curve was used to analyze the differences between the groups (n = 10). D Flow cytometry was used to detect immune cell subpopulations (M1 and M2 macrophages, Tregs, CD4+ and CD8+ T cells) in the brain tumor immune microenvironment of control group, MDK overexpression group, and MDK overexpression combined with iMDK treatment group (n = 3). E Multiple immunofluorescence staining was used to detect the expression and distribution characteristics of MDK, CD206, and CXCL1 molecules in control group, MDK overexpression group, and MDK overexpression combined with iMDK treatment group (n = 3). F Molecular mechanisms diagram of immune evasion in GBM with EGFRvIII mutation. *, ** and **** indicate P < 0.05, P < 0.01 and P < 0.0001, respectively. unpaired two-tailed Student’s t test. The overall survival of mice was analyzed for prognosis using the Kaplan-Meier method.