Supplementary Materials

Supplementary Material for:

Development of a stress response therapy targeting aggressive prostate cancer

Hao G. Nguyen, Crystal S. Conn,* Yae Kye, Lingru Xue, Craig M. Forester, Janet E. Cowan, Andrew C. Hsieh, John T. Cunningham, Charles Truillet, Feven Tameire, Michael J. Evans, Christopher P. Evans, Joy C. Yang, Byron Hann, Constantinos Koumenis, Peter Walter, Peter R. Carroll, Davide Ruggero*

*Corresponding author. Email: crystal.conn{at}ucsf.edu (C.S.C.); davide.ruggero{at}ucsf.edu (D.R.)

Published 2 May 2018, Sci. Transl. Med. 10, eaar2036 (2018)
DOI: 10.1126/scitranslmed.aar2036

This PDF file includes:

  • Materials and Methods
  • Fig. S1. MycTg and PTEN loss cooperate for aggressive PCa development in mice.
  • Fig. S2. The UPR is activated in murine PCa.
  • Fig. S3. PERK loss blocks PCa progression and decreases P-eIF2α expression.
  • Fig. S4. Loss of P-eIF2α activity by ISRIB shows no toxicity and does not substantially alter infiltrating immune cells.
  • Fig. S5. Inhibition of P-eIF2α activity by ISRIB does not affect human prostatic cell lines’ growth.
  • Fig. S6. PCa tissue from TMA shows specificity of protein expression in benign and tumor cells.
  • Fig. S7. Treatment with ISRIB or ATF4 siRNA results in increased apoptosis within metastatic tumor.
  • Fig. S8. A PDX was generated to recapitulate mCRPC.
  • References (49–54)

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Other Supplementary Material for this manuscript includes the following:

  • Table S1 (Microsoft Excel format). MRI tumor volumes during treatment in GEMMs.