Fig. 3. Triacylglyceride formation protects cells from ferroptosis.

Quantification of PI-positive Caki-1 cells treated with 2 μM erastin for 18 h using flow cytometry. Cells were pretreated with a vehicle or iDGAT1/2 with 0.3 mM hydroxyurea (a), 1 mM thymidine (b), 0.035 μg/ml colcemid (c), or 200 nM nocodazole (d) for 24 h. Lipid peroxidation measurement in Caki-1 cells treated with 2 μM erastin for 8 h. Cells were pretreated with a vehicle or iDGAT1/2 with 0.3 mM hydroxyurea (e), 1 mM thymidine (f), 0.035 μg/ml colcemid (g), or 200 nM nocodazole (h) for 24 h. WT, DGAT DKO1, and DGAT DKO2 Caki-1 cells were pretreated with cell cycle inhibitors for 24 h. Shown are the populations of PI-positive cells after treatment with 2 μM erastin for 18 h (i–l) and those with lipid peroxidation after treatment with 2 μM erastin for 8 h (m–p). q, r, The populations of PI-positive Caki-1 cells pretreated with a vehicle or iDGAT1/2 for 24 h after treatment with 2 μM erastin for 18 h (q) and lipid peroxidation after treatment with 2 μM erastin for 8 h (r). s, t WT, sgCDK1-2, and sgCDK1-3 Caki-1 cells were pretreated with iDGAT1/2 for 24 h. The populations of PI-positive cells after treatment with 2 μM erastin for 18 h (s) and lipid peroxidation after treatment with 2 μM erastin for 8 h (t) are shown. Mean ( ± SD) values are shown. n = 3. n indicates independent repeats (unpaired, two-tailed t-test). Source data are provided as a Source Data file.