Supplementary Materials

Supplementary Materials for:

Cell type–specific abundance of 4EBP1 primes prostate cancer sensitivity or resistance to PI3K pathway inhibitors

Andrew C. Hsieh,* Hao G. Nguyen, Lexiaochuan Wen, Merritt P. Edlind, Peter R. Carroll, Won Kim, Davide Ruggero*

*Corresponding author. E-mail: ahsieh{at}fredhutch.org (A.C.H.); davide.ruggero{at}ucsf.edu (D.R.)

This PDF file includes:

  • Fig. S1. Absolute quantification of basal epithelial cells and luminal epithelial cells after treatment with MLN0128.
  • Fig. S2. qPCR phenotyping of distinct sorted epithelial cell populations in wild-type and PTENL/L mice.
  • Fig. S3. Efficiency of PTEN deletion and the phosphorylation and localization of 4EBP1 in basal and luminal epithelial cells in vivo.
  • Fig. S4. Western blot analysis of translation initiation factors and regulators in wild-type and PTENL/L basal and luminal epithelial cells.
  • Fig. S5. 4EBP1M does not affect normal prostate homeostasis but impedes prostate cancer initiation and progression.
  • Fig. S6. Effect of PTEN loss and 4EBP1M expression on absolute number of basal and luminal epithelial cells.
  • Fig. S7. Expression of 4EBP1 endows resistance to MLN0128 in LHS PTEN KD cell lines.
  • Fig. S8. Phosphorylated AKT (Ser473) immunohistochemistry of prostate tumors and serum PSA concentrations from patients before and after treatment with BKM120.
  • Table S1. qPCR oligonucleotide sequences.

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Citation: A. C. Hsieh, H. G. Nguyen, L. Wen, M. P. Edlind, P. R. Carroll, W. Kim, D. Ruggero, Cell type–specific abundance of 4EBP1 primes prostate cancer sensitivity or resistance to PI3K pathway inhibitors. Sci. Signal. 8, ra116 (2015).

© 2015 American Association for the Advancement of Science