Supplementary Materials

Supplementary Material for:

Ibrutinib inactivates BMX-STAT3 in glioma stem cells to impair malignant growth and radioresistance

Yu Shi, Olga A. Guryanova, Wenchao Zhou, Chong Liu, Zhi Huang, Xiaoguang Fang, Xiuxing Wang, Cong Chen, Qiulian Wu, Zhicheng He, Wei Wang, Wei Zhang, Tao Jiang, Qing Liu, Yaping Chen, Wenying Wang, Jingjing Wu, Leo Kim, Ryan C. Gimple, Hua Feng, Hsiang-Fu Kung, Jennifer S. Yu, Jeremy N. Rich, Yi-Fang Ping,* Xiu-Wu Bian,* Shideng Bao*

*Corresponding author. Email: baos{at}ccf.org (S.B.); bianxiuwu{at}263.net (X.-W.B.); pingyifang{at}126.com (Y.-F.P.)

Published 30 May 2018, Sci. Transl. Med. 10, eaah6816 (2018)
DOI: 10.1126/scitranslmed.aah6816

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Ibrutinib treatment inhibits GBM growth and prolongs animal survival.
  • Fig. S2. Ibrutinib penetrates into mouse brains and has no severe systemic side effects.
  • Fig. S3. Ibrutinib treatment is effective for most GBMs tested.
  • Fig. S4. Ibrutinib treatment targets GSCs but not NPCs in vivo.
  • Fig. S5. Ibrutinib is more effective at targeting GSCs than NSTCs.
  • Fig. S6. Ibrutinib treatment inhibits BMX-mediated STAT3 activation in GSCs.
  • Fig. S7. Ectopic expression of constitutively active STAT3 largely rescues GSC maintenance disrupted by ibrutinib.
  • Fig. S8. JAK2 mediates STAT3 activation in NPCs, whereas BMX interacts with gp130 to mediate STAT3 activation in GSCs.
  • Fig. S9. Forced expression of SOCS3 inhibits JAK2-mediated STAT3 activation in NPCs.
  • Table S1. Pathological and molecular features of patient-derived GSCs used in this study.
  • Table S2. Expression of BMX and pBMX-Y40 and the pathological characteristics of human GBMs used in this study.
  • Table S3. Sequences of shRNAs used in this study.
  • References (3840)

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