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. Author manuscript; available in PMC: 2023 Feb 17.
Published in final edited form as: Mol Cancer Ther. 2021 Jun 22;20(9):1692–1701. doi: 10.1158/1535-7163.MCT-21-0210

Figure 4. MSU38225 dampens the anti-oxidative response and inhibits cell growth in cancer cells in a Nrf2-dependent manner.

Figure 4.

A. A549 cells were treated with MSU38225 for 24 hours. Cells were stimulated with 250 μM tert-butyl hydroperoxide (tBHP) for 15 minutes. Reactive oxygen species (ROS) production was detected using DCFDA as an indicator. Experiment was done in triplicate and repeated in 3 independent assays. *, p<0.05 vs. tBHP+DMSO control. B. Cell viability was analyzed using a MTT assay in four cell lines after 72-hour treatment with MSU38225. C. A549, H460 and A427 cells were plated in 0.6% soft agar for 7 days. Colonies larger than 50 μm in diameter were quantified. The experiment was done in triplicate and repeated twice. *, p<0.05 vs. DMSO control. Data shown as mean±SD. D. The efficacy of Nrf2 deletion in A549 cells was confirmed with western blotting. E. Nrf2 WT and KO A549 cells were treated with 5 μM MSU38225 for 24 hours. Cells were stimulated with 250 μM tert-butyl hydroperoxide (tBHP) for 15 minutes. Reactive oxygen species (ROS) production was detected. Experiment was done in triplicate and repeated in 3 independent assays. *, p<0.05 vs. tBHP+DMSO control; ns, p>0.05 vs. tBHP+DMSO control. F. Cell viability was measured using MTT assay in Nrf2 WT vs. KO A549 cells after 72-hour treatment with MSU38225. *, p<0.05 vs. Nrf2 WT at the same concentration.