Fig. 7: TRIM22 is highly expressed in GBM samples and correlates with other clinical parameters associated with higher grade glioma.
From: TRIM22 activates NF-κB signaling in glioblastoma by accelerating the degradation of IκBα
a Images of TRIM22 IHC performed on WHO grade II–IV glioma tissue microarrays and nonneoplastic brain tissues (NBT). Representative image of NBT was from the frontal lobe. Scale bar = 100 μm (top) or 50 μm (bottom). For glioma tissue microarrays, scale bar = 200 μm (top) or 50 μm (bottom). b Graphic representation of scoring performed on IHC staining for TRIM22 in primary samples from glioma tissue microarrays and NBTs. c Western blot analysis of TRIM22 protein levels in primary glioma tissues (n = 12) and nonneoplastic brain tissue samples (n = 3). d, e In vivo bioluminescence imaging and quantification of modified GBM#P3 and GSC#BG5 cells derived xenografts at the indicated time points. f Kaplan–Meier survival analysis performed with survival data from indicated cells. Log-rank test, P < 0.05. g A graphical model for TRIM22-mediated NF-κB activation and GBM growth, showing interaction of TRIM22 with critical components of the pathway, including IκBα which normally sequesters the transcription activating complex in the cytoplasm. TRIM22 targets IκBα for proteasomal-mediated degradation and activates the IKK complex through K63-linked ubiquitination of IKKγ/NEMO, which leads to further disruption of IκBα from the complex. Student’s t test: n.s. not significant, *P < 0.05, **P < 0.01, ***P < 0.001.
