Fig. 2: Enhanced FAO drives the aggressive growth of radioresistant GBM cells.
From: Fatty acid oxidation fuels glioblastoma radioresistance with CD47-mediated immune evasion
a RR Gl261 cells (5 × 106) were inoculated subcutaneously into both flanks of mice and when the tumor reached the sizes 200 mm3, palmitate (100 μl of 25 μM or 0.05% BSA as solvent control) were administrated twice 72 h apart via intratumoral injection. Tumor volumes (P = 0.0077) and weights (P = 0.0104) were measured at the end of experiment (Day 18; n = 10). A paired two-tailed t-test was applied. b ATP luminesce concentration of WT and RR GL261 cells treated by an indicated concentration of palmitate. n = 3. An unpaired two-tailed t-test was applied. c FAO activity quantified by the conversion of 3H palmitic acid to 3H2O over 6 h using radioactive isotope tracers ([9,10-3H(N)]-palmitic acid [0.5 µCi (~9.3 pmol)]) (n = 3 per cell line) in parental WT and RR GBM cells (U251, U87, A172, and GL261). An unpaired two-tailed t-test was applied. The concentration of acetyl-CoA (d), glucose uptake (e), and l-lactate (f) was measured in WT and RR GBM cells (U251, U87, A172, and GL261; n = 3 per cell line). g Mitochondria number counts in parental WT and RR GBM cells (U251 and GL261; n = 6 per cell line; scale bar = 10 µm). h The basal and spared oxygen consumption rate (OCR) generated with FCCP, a potent uncoupler of mitochondrial oxidative phosphorylation in WT and RR U251 (P = 0.0016), U87 (P = 0.0004), A172 (P = 1.74E-5), and GL261 cells (P = 1.48E-7) (n = 9). An unpaired two-tailed t-test was applied in b–h. Lipid accumulation (i), OCR (j), and ATP generation (k) in WT and RR GBM cells treated with or without CPT1 inhibitor ET (in i and k, ET = 200 µM, 24 h, n = 4; in j, ET = 40 µM, 0.5 h, n = 9). Results represent the means ± SD; ANOVA two-way test was applied; WT wildtype, RR radioresistant, ET etomoxir. Source data are provided as a Source Data file.
