Figure 6.
RSL3 potentiates BTZ activity by abrogating xCT upregulation upon BTZ treatment and attenuating GSH levels in t(4;14)-positive MM. (A-B) Western blotting analysis of t(4;14)-positive NCI-H929 and OPM-2 cells and t(4;14)-negative U-266 cells with BTZ single treatment (A) or RSL3 combination treatment (B) for 48 hours. GAPDH was used as the internal control, and the intensities were measured using ImageJ. (C) Cellular reduced glutathione levels were detected in t(4;14)-positive NCI-H929 and OPM-2 cells and t(4;14)-negative U-266 cells treated with BTZ or RSL3 alone or together for 24 hours. (D-E) Relative cell viability were detected in t(4;14)-positive NCI-H929 and OPM-2 cells treated with BTZ or RSL3 alone or together for 24 hours in the presence of NAC (a GSH precursor) (D) or trolox (a lipid ROS scavenger) (E). ns, not significant; P > .05, ∗ P <0 .05, ∗∗ P < .01, and ∗∗∗ P < .001.

RSL3 potentiates BTZ activity by abrogating xCT upregulation upon BTZ treatment and attenuating GSH levels in t(4;14)-positive MM. (A-B) Western blotting analysis of t(4;14)-positive NCI-H929 and OPM-2 cells and t(4;14)-negative U-266 cells with BTZ single treatment (A) or RSL3 combination treatment (B) for 48 hours. GAPDH was used as the internal control, and the intensities were measured using ImageJ. (C) Cellular reduced glutathione levels were detected in t(4;14)-positive NCI-H929 and OPM-2 cells and t(4;14)-negative U-266 cells treated with BTZ or RSL3 alone or together for 24 hours. (D-E) Relative cell viability were detected in t(4;14)-positive NCI-H929 and OPM-2 cells treated with BTZ or RSL3 alone or together for 24 hours in the presence of NAC (a GSH precursor) (D) or trolox (a lipid ROS scavenger) (E). ns, not significant; P > .05, ∗ P <0 .05, ∗∗ P < .01, and ∗∗∗ P < .001.

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