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Sci. Signal., 15 December 2009
[DOI: 10.1126/scisignal.2000446]

Supplementary Materials for:

EGFR Signaling Through an Akt-SREBP-1–Dependent, Rapamycin-Resistant Pathway Sensitizes Glioblastomas to Antilipogenic Therapy

Deliang Guo, Robert M. Prins, Julie Dang, Daisuke Kuga, Akio Iwanami, Horacio Soto, Kelly Y. Lin, Tiffany T. Huang, David Akhavan, M. Benjamin Hock, Shaojun Zhu, Ava A. Kofman, Steve J. Bensinger, William H. Yong, Harry V. Vinters, Steve Horvath, Andrew D. Watson, John G. Kuhn, H. Ian Robins, Minesh P. Mehta, Patrick Y. Wen, Lisa M. DeAngelis, Michael D. Prados, Ingo K. Mellinghoff, Timothy F. Cloughesy, Paul S. Mischel*

*To whom correspondence should be addressed. E-mail: pmischel{at}mednet.ucla.edu

This PDF file includes:

  • Fig. S1. Nuclear SREBP-1 staining in 12 control GBM patients.
  • Fig. S2. Effect of PTEN on SREBP-1.
  • Fig. S3. Proliferation rates of GBMs (T98, LN229, U373, U138, U87) and epidermoid carcinoma cell line (A431).
  • Fig. S4. Effect of 25-hydroxycholesterol (25-HC) on SREBP-1 cleavage and ACC and FAS abundance.
  • Fig. S5. Inhibition of mTORC1 signaling with rapamycin does not prevent SREBP-1 cleavage in cancer cells with highly abundant EGFR.
  • Fig. S6. p-PDGFR and p-Met are also associated with p-Akt and nuclear SREBP-1 staining in glioblastoma tissue microarrays and Met activation can promote SREBP-1 cleavage in glioblastoma cells in vitro.
  • Fig. S7. Effect of 25-hydroxycholesterol (25-HC) on tumor viability.
  • Fig. S8. Lipogenesis inhibitors induce cell death in other cancer types with abundant EGFR.
  • Fig. S9. Analysis of poly(ADP-ribose) polymerase (PARP) cleavage confirms that inhibitors of lipogenesis promote apoptotic cell death.
  • Fig. S10. Effect of PTEN reconstitution on cellular response to 25-HC.
  • Fig. S11. Palmitate, a product of FAS, significantly rescues C75-mediated cell death.
  • Fig. S12. Effects of atorvastatin and C75 on Ki67 proliferation index in vivo.
  • Fig. S13. Effects of atorvastatin or C75 alone or in combination, on the growth of U87 or isogenic U87-EGFRvIII tumors in vivo.
  • Table S1. EGFR inhibition and lapatinib drug concentration in tumor.
  • Table S2. Immunohistochemical staining of proteins in tissue microarrays of GBM samples and adjacent normal brain.
  • Table S3. Coexpression of immunohistochemical markers in GBM samples on tissue microarray.
  • Table S4. Signaling pathway marker correlations from GBM samples on tissue microarray.

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Citation: D. Guo, R. M. Prins, J. Dang, D. Kuga, A. Iwanami, H. Soto, K. Y. Lin, T. T. Huang, D. Akhavan, M. B. Hock, S. Zhu, A. A. Kofman, S. J. Bensinger, W. H. Yong, H. V. Vinters, S. Horvath, A. D. Watson, J. G. Kuhn, H. I. Robins, M. P. Mehta, P. Y. Wen, L. M. DeAngelis, M. D. Prados, I. K. Mellinghoff, T. F. Cloughesy, P. S. Mischel, EGFR Signaling Through an Akt-SREBP-1–Dependent, Rapamycin-Resistant Pathway Sensitizes Glioblastomas to Antilipogenic Therapy. Sci. Signal. 2, ra82 (2009).

© 2009 American Association for the Advancement of Science


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Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882