Fig. 1

Paclitaxel-tolerant persister cancer cells (PCC) have a metabolic shift to fatty acid oxidation. A PCC was made from HN3 and HN4 cells using 10 nM paclitaxel for 6 days and then was maintained without paclitaxel for 38 days before the second 6-day drug treatment to get re-derived PCC. Scale bar 10 μm. B Cell viability was measured using cell counting kit-8 (CCK-8) assay after 10 nM paclitaxel treatment for 48 h in parental cells (ctr) and PCC. Data are means and s.d. from three technical replicates. **P < 0.01, ***P < 0.001 relative to DMSO control. C Immunostaining of α-tubulin (green) in HN3 and HN4 parental cells and PCC. Nuclei (blue) were stained with 4′,6-diamidino-2-phenylindole (DAPI). Scale bar 10 μm. D and E Extracellular acidification rate (ECAR) assay in HN3 and HN4 parental cells and PCC. ECAR was measured using a microplate fluorometer at 15 min intervals, and the glycolysis effect was examined from ECAR assay at 120 min. **P < 0.01 relative to parental cells. F Cellular glutamate was quantified in parental cells and PCC. **P < 0.01 relative to parental cells. G-I Free fatty acids and fatty acid oxidation (FAO) were measured in parental cells and PCC. FAO was quantified via assessing changes in oxygen consumption (OCR) and calculated as a formula (sample untreated with etomoxir minus sample treated with 10 μM etomoxir). Data are means and s.d. and from three technical replicates. **P < 0.01 relative to parental cells. J-L Oil red O staining, immunoblotting, and lipid droplet staining in parental cells and PCC. Scale bars 100 μm (J) and 10 μm (L)