Fig. 2: Rimonabant combined with erastin/RSL3 significantly inhibited TNBC cell growth by inducing ferroptosis and cell cycle arrest. | Cell Death & Disease

Fig. 2: Rimonabant combined with erastin/RSL3 significantly inhibited TNBC cell growth by inducing ferroptosis and cell cycle arrest.

From: Inhibition of cannabinoid receptor type 1 sensitizes triple-negative breast cancer cells to ferroptosis via regulating fatty acid metabolism

Fig. 2

A MDA-MB-231 cells were pretreated with the indicated cell death inhibitors for 1 h, and then cells were added with rimonabant (SR, 10 μM), erastin (5 μM) and RSL3 (0.5 μM) as single agents or drug combinations for an additional 72 h. Cell viability (CCK-8) is presented as percentage of untreated cells. B The level of GSH was determined after treated with rimonabant (SR, 10 μM), erastin (5 μM) and RSL3 (0.5 μM) as single agents or drug combinations for 48 h in MDA-MB-231 cells. **p < 0.01 (one-way ANOVA). C–F MDA (C), 4-HNE (D), lipid peroxidation (E) and cytosolic ROS (F) production of MDA-MB-231 cells treated as B Histograms show the production of MDA, 4-HEN, relative fold change of lipid ROS and cytosolic ROS (right panel). ns (no significance), *p < 0.05, **p < 0.01 (one-way ANOVA). G, H The cell cycle distributions of MDA-MB-231 and HCC1937 cells were treated as B. Cell cycle was evaluated by flow cytometry after staining with propidium iodide (PI). Histograms show the cell cycle distributions of treated MDA-MB-231 and HCC1937 cells H. **p < 0.01 versus the vehicle (t-test). I Representative western blotting assays of MDA-MB-231 and HCC1937 cells were treated as B with the indicated antibodies. Data shown are mean ± SD of triplicate measurements that were repeated three times with similar results.

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