Supplementary Data and Methods from Modulation of Bax and mTOR for Cancer Therapeutics

Authors:
  • RLRui Li
    Rui Li
  • CDChunyong Ding
    Chunyong Ding
  • JZJun Zhang
    Jun Zhang
  • MXMaohua Xie
    Maohua Xie
  • DPDongkyoo Park
    Dongkyoo Park
  • YDYe Ding
    Ye Ding
  • GCGuo Chen
    Guo Chen
  • GZGuojing Zhang
    Guojing Zhang
  • MGMelissa Gilbert-Ross
    Melissa Gilbert-Ross
  • WZWei Zhou
    Wei Zhou
  • AMAdam I. Marcus
    Adam I. Marcus
  • SSShi-Yong Sun
    Shi-Yong Sun
Open Access
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Abstract
Figure S1. Bak BH3 peptide position in Bak protein. Figure S2. Dephosphorylation of Bax by lambdaPPase in vitro. Figure S3. Bax activators CYD-2-11 and SMBA1 failed to induce Bak oligomerization. Figure S4. Analysis of CYD-2-11 toxicity in vivo. Figure S5. CYD-2-11 has no significant effect on total Bax expression in SCLC PDX models. Figure S6. Toxicity analysis of CYD-2-11 in 2 PDX models. Figure S7. Bax phosphorylation is up-regulated in KRAS driven lung cancer. Figure S8. Quantification of tumor burden. Figure S9. H&E staining of normal tissues from various organs after CYD-2-11 treatment of KL mice. Figure S10. The dual PI3K/mTOR inhibitor BEZ235 inhibits ATK activity leading to down-regulation of Bax phosphorylation. Figure S11. CYD-2-11 synergizes with RAD001 to reverse rapalog resistance of lung cancer cells. Figure S12. RAD001 and CYD-2-11 did not affect total Bax in A549 xenografts. Figure S13. Toxicity analysis following treatment with RAD001, CYD-2-11 or in combination in A549 xenografts. Figure S14. CYD-2-11 synergizes with RAD001 against lung cancer in PDX model.