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. 2021 Oct 5;125(11):1511–1522. doi: 10.1038/s41416-021-01566-9

Fig. 6. The characteristics of persister cells and the effect of RSL3 (glutathion peroxidase 4 [GPX4] inhibitor) on persister cells in other cell lines (epidermal growth factor receptor (EGFR)-mutant lung cancer cell line PC9 and mutational imatinib-resistant gastrointestinal stromal tumour [GIST] cell line GIST-R8).

Fig. 6

a A small fraction of PC9 cells survived through ≥9 days of treatment with 2 μM gefitinib or 10 μM 5-fluorouracil (FU). Scale bars, 200 μm. b Intracellular concentration of glutathione (GSH) in PC9 parental and gefitinib-derived persister or 5-FU-derived persister cells measured by GSH-Glo assay. Data represent mean ± standard deviation (SD) (n = 4), *P < 0.05. c Western blotting analysis of GPX4 in parental and gefitinib-derived persister or 5-FU-derived persister cells. d Fractional viability of PC9 parental cells, gefitinib-derived persister cells and 5-FU-derived persister cells treated with the indicated concentrations of RSL3. Cell viability was determined by Cell-titer Glo. Data represent mean ± SD (n = 6), *P < 0.05. e Intracellular concentration of GSH in GIST-T1 parental cells and the mutational imatinib-resistant GIST cell line, GIST-R8 measured by GSH-Glo assay (Promega). Data represent mean ± SD (n = 4), *P < 0.05. f Fractional viability of GIST-T1 parental cells and GIST-R8 cells treated with indicated concentrations of RSL3. Cell viability was determined by Cell-titer Glo Assay. Data represent mean ± SD (n = 6), *P < 0.05.