Fig. 5: GOT1 inhibition promotes labile iron release.
From: GOT1 inhibition promotes pancreatic cancer cell death by ferroptosis
a Calcein-AM histogram (a) and mean fluorescence intensity (MFI) (***P = 0.0002) upon 5 days of GOT1 knockdown, n = 3 biological replicates. b Visualization and quantification of GOT1 knockdown cells treated with the iron probe RhoNox-1, n = 3 biological replicates. **P = 0.0013. Scale bars represent 200 μm. Image is representative of two independent experiments. c ICP-MS (Inductively coupled plasma mass spectrometry) measurements of iron in subcutaneous and orthotopic tumors following GOT1 knockdown, n = 4 tumors, *P = 0.0191 and **P = 0.0036. d Cell viability normalized to vehicle of cells co-treated with 32 nM RSL3 and increasing doses of DFO, n = 2 biological replicates. e Cell viability dose response to FINO2 with or without 200 µM ferric ammonium citrate (FAC), n = 3 biological replicates. Cell viability of FINO2 with 200 µM FAC (ferric ammonium citrate) (f) or the indicated rescue conditions n = 3 biological replicates, ****P = < 0.0001. g Western of autophagy markers following GOT1 knockdown representative of two independent experiments. h Cell viability in cells co-treated with RSL3 and siNCOA4 following GOT1 knockdown, n = 3 biological replicates, ****P ≤ 0.0001. i Model describing the GOT1-mediated potentiation of ferroptosis through ferritinophagic iron release. Error bars represent mean ± SD. Two-tailed unpaired T-test or one-way ANOVA. Source data are provided as a Source Data file.
