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. Author manuscript; available in PMC: 2022 Mar 1.
Published in final edited form as: Cancer Discov. 2021 Apr 20;11(9):2334–2353. doi: 10.1158/2159-8290.CD-20-1114

Figure 5. RB loss protects against ROS through increased glutathione synthesis.

Figure 5.

(A) Glutathione synthesis pathway highlighting increased genes after RB knockdown (red) and altered metabolites after RB knockdown (blue). Validation of increased relative mRNA expression of genes required for glutathione metabolism in C4-2, LN95, MCF7, and H1299 derived isogenic models after RB1 depletion and after transient knockdown of RB in UMUC3 models. (B) Validation of protein increase in C4-2-shCon C4-2-shRB. (C) Total glutathione in C4-2, LN95, MCF7, and H1299 derived isogenic models after RB1 depletion and after transient knockdown of RB in UMUC3 models. (D) ROS assay in C4-2, LN95, and MCF7 derived isogenic models. Menadione was used at 50 μM as a positive control for inducing ROS. (E) ROS assay after multiple timepoints of doxorubicin treatment in C4-2 and LN95 derived isogenic models. *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001.