Supplementary Materials

Supplementary Materials for:

ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling

Jun Wang, Clay Rouse, Jeff S. Jasper, Ann Marie Pendergast*

*Corresponding author. E-mail: ann.pendergast{at}duke.edu

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  • Fig. S1. ABL family protein abundance is increased in breast cancer cells with enhanced bone metastatic activity, and ABL1/ABL2 depletion does not affect proliferation in vitro.
  • Fig. S2. ABL kinases promote breast cancer cell invasion.
  • Fig. S3. Depletion of ABL kinases does not inhibit metastasis of 4175 breast cancer cells, which show tropism to the lung.
  • Fig. S4. Treatment of breast cancer cells with imatinib but not GNF5 promotes ERK activation.
  • Fig. S5. CXCL12- and IGF-1–mediated survival pathways are independent of ABL kinases.
  • Fig. S6. Depletion of ABL kinases in SKBR3 breast cancer cells decreases tumor-induced osteoclast activation.
  • Fig. S7. IL-6 affects RANKL and OPG expression in osteoblasts.
  • Fig. S8. Quality control and global statistics of RNAseq analysis for transcriptome comparison of control versus ABL1/ABL2 knockdown breast cancer cells.
  • Fig. S9. ABL kinases increase TAZ protein abundance and STAT5 phosphorylation.
  • Fig. S10. Depletion of ABL kinases reduces the abundance of TAZ in the nucleus.
  • Fig. S11. Allosteric inhibition of ABL kinase activity decreases TAZ protein abundance.
  • Fig. S12. ABL2 mRNA expression positively correlates with TAZ mRNA expression in invasive breast cancer patients.
  • Fig. S13. Depletion of ABL kinases decreases the binding of TAZ to target genes.
  • Fig. S14. Depletion of ABL kinases does not affect YAP1 protein abundance, localization, or tyrosine phosphorylation in breast cancer cells.
  • Fig. S15. Expression of a constitutively active STAT5 mutant increases mRNA expression of MMP1, IL6, and TNC.
  • Fig. S16. Potential interdependence of TAZ and STAT5 in breast cancer cells.
  • Table S1. Differentially expressed genes in control and ABL1/ABL2 knockdown breast cancer cells.

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Citation: J. Wang, C. Rouse, J. S. Jasper, A. M. Pendergast, ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling. Sci. Signal. 9, ra12 (2016).

© 2016 American Association for the Advancement of Science