Supplementary Materials

Supplementary Material for:

RON kinase: A target for treatment of cancer-induced bone destruction and osteoporosis

Kelsi Andrade, Jaime Fornetti, Ling Zhao, Scott C. Miller, R. Lor Randall, Neysi Anderson, Susan E. Waltz, Mark McHale, Alana L. Welm*

*Corresponding author. Email: alana.welm{at}

Published 25 January 2017, Sci. Transl. Med. 9, eaai9338 (2017)
DOI: 10.1126/scitranslmed.aai9338

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Tumor cell proliferation does not differ between control and MSP-expressing tumor cells or in the absence of host RON.
  • Fig. S2. The number of osteoclasts is similar between WT and RON TK−/− tumor-bearing bones.
  • Fig. S3. The number of osteoclasts is similar between normal, non–tumor-bearing WT and RON TK−/− bones.
  • Fig. S4. Lack of RON signaling does not affect bone formation.
  • Fig. S5. OSI-296 treatment does not alter osteolysis associated with PyMT control tumors.
  • Fig. S6. Treatment with OSI-296 does not affect osteoclast number or bone formation.
  • Fig. S7. Tumor growth is reduced by OSI-296 but not by BMS-777607/ASLAN002.
  • Fig. S8. muRANK-Fc treatment effectively reduces osteoclast numbers but does not affect MSP-induced osteolysis.
  • Fig. S9. MSP-induced osteolysis occurs separately from RANKL and TGFβ signaling.
  • Fig. S10. MSP promotes survival of mature osteoclasts, but not differentiation, through SRC.
  • Fig. S11. SRC family kinase levels are not significantly regulated by MSP.
  • Fig. S12. MSP protein is expressed in breast cancer bone metastasis samples from patients.
  • Fig. S13. MSP gene expression is up-regulated in multiple myeloma and lung adenocarcinoma.
  • Table S1. Individual patient demographic and treatment information plus CTX and BSAP levels.
  • Reference (55)

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