Supplementary Materials

Supplementary Materials for:

The GAS6-AXL signaling network is a mesenchymal (Mes) molecular subtype–specific therapeutic target for ovarian cancer

Jane Antony, Tuan Zea Tan, Zoe Kelly, Jeffrey Low, Mahesh Choolani, Chiara Recchi, Hani Gabra, Jean Paul Thiery, Ruby Yun-Ju Huang*

*Corresponding author. Email: ruby_yj_huang{at}nuhs.edu.sg

This PDF file includes:

  • Fig. S1. AXL rank and expression in GEMS and EMT phenotype.
  • Fig. S2. AXL signaling in GEMS has divergent biological consequences.
  • Fig. S3. GAS6-AXL signaling relies on MEK-ERK pathway to promote motility in Mes-subtype tumor cells.
  • Fig. S4. Epi-A cells show membrane modulation of AXL-RTK networks and DUSP4 regulation of the pERK response.
  • Fig. S5. Mes- subtype cells are more sensitive to AXL-specific inhibition.
  • Fig. S6. AXL mediates the phenotypic transitions of EMT.
  • Fig. S7. The AXL gene signature is enriched in Mes-subtype tumors and correlates with worse prognosis in patients.
  • Fig. S8. Full-length blots.
  • Table S1. High AXL expression predicts poor prognosis in ovarian cancer in multivariate analysis.
  • Table S2. High AXL expression predicts poor prognosis in ovarian cancer even when accounting for the effect arising from the GEMS.
  • Table S3. The AXL gene signature is prognostically relevant in ovarian cancer.

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Citation: J. Antony, T. Z. Tan, Z. Kelly, J. Low, M. Choolani, C. Recchi, H. Gabra, J. P. Thiery, R. Y.-J. Huang, The GAS6-AXL signaling network is a mesenchymal (Mes) molecular subtype–specific therapeutic target for ovarian cancer. Sci. Signal. 9, ra97 (2016).

© 2016 American Association for the Advancement of Science