Fig. 4: CXCR3 regulates mitochondrial function through p-STAT3 signaling.

A The mRNA expression of STAT3 in CXCR3high and CXCR3low GBMs from a publicly available database. (TCGA, n = 166). B Western blot analysis of total STAT3 and Phospho-STAT3 (p-STAT3) expression in U87 cells expressing shCtrl and shCXCR3. C Relative cell viability in U87 and U251 cells treated with the CXCR3 inhibitor AMG487 for 72 hours, withglioblastoma stem cell or without the addition of low-dose or high-dose STAT3 activator. The STAT3 activator was used to rescue the effects of CXCR3 inhibition on downstream STAT3 activity. D A hypothetical diagram depicting the proposed mechanism whereby increased CXCR3 activation may lead to enhanced phosphorylation and activation of STAT3 in the mitochondria, which in turn promotes STAT3-mediated redox balance and enhances cancer metabolism as indicated by the increased OCR in GBM. Figure created using BioRender (https://biorender.com). (ROS reactive oxygen species, OCR oxygen consumption rate) Error bars indicate mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns (no statistical significance).