Fig. 3: Targeting POLQ renders gastric cancer cells more vulnerable to ferroptosis. | Cell Death & Disease

Fig. 3: Targeting POLQ renders gastric cancer cells more vulnerable to ferroptosis.

From: POLQ inhibition attenuates the stemness and ferroptosis resistance in gastric cancer cells via downregulation of dihydroorotate dehydrogenase

Fig. 3

A High POLQ expression correlates with resistance to ferroptosis inducers (RSL3, ML162, and ML210) in cancer cells. Plotted data were mined from the CTRP database. B Cell viability in control and POLQ- knockdown GC cells treated with RSL3 (10 µM) or erastin (15 µM) for 24 h. C, D Respective lipid peroxidation levels were assessed and calculated by flow cytometry using BODIPY C11. E Control and POLQ- knockdown GC cells were collected for lipid peroxidation measurement (scale bar = 20 μm). F The mRNA levels of PTGS2 were detected in control and POLQ- knockdown GC cells treated with RSL3 (5 µM) or erastin (10 µM) for 24 h. G Cell viability in control and POLQ- knockdown GC cells treated with 1-stearoyl-2-15(S)-HpETE-sn-glycero-3-PE for 24 h. H Control and POLQ- knockdown GC cells were incubated with vehicle or 1-stearoyl-2-15(S)-HpETE-sn-glycero-3-PE for 24 h and stained with Calcein AM reagent and the representative images were acquired by fluorescence microscope (scale bar = 200 μm). I Cells were fixed and stained for γ–H2AX, 24 h after treated with vehicle, RSL3 or erastin (scale bar = 20 μm). Results are shown as mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001.

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