Fig. 8: Clinical relevance of PSMD14 and BCKDK in GBM patients. | Cell Death & Differentiation

Fig. 8: Clinical relevance of PSMD14 and BCKDK in GBM patients.

From: Targeting the PSMD14-BCKDK pathway overcomes immune suppression and enhances CAR-NK infiltration in glioblastoma

Fig. 8: Clinical relevance of PSMD14 and BCKDK in GBM patients.The alt text for this image may have been generated using AI.

A Representative multiplex IF images of two GBM cases showing the strategy for tumor-infiltrating lymphocyte (TIL) identification based on CD56 and CD8 expression; each marker is displayed in a distinct color, scale bars: 50 μm (overview), 25 μm (boxed area). Quantification of CD8⁺ T cells (B) and CD56⁺ NK cells (C) in GBM tissues with high (n = 73) or low (n = 41) PSMD14 expression, assessed by multiplex IF staining. All data are mean ± SEM. P values were calculated using unpaired two-tailed Student’s t test. D Representative IHC images of PSMD14 and BCKDK in human GBM samples, 200 μm (overview), 25 μm (boxed area). Kaplan–Meier survival analysis of GBM patients (n = 114), stratified by PSMD14 (E) or BCKDK (F) expression (log-rank test, P < 0.0001). G Schematic illustration of the PSMD14/BCKDK/IGF2BP3 positive feedback circuit, which stabilizes SLC7A5/SLC7A8 mRNAs to promote GBM-driven BCAA acquisition, suppress NK cell activation, and exacerbate the formation of an immunosuppressive TME.

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