The Rho Exchange Factors Vav2 and Vav3 Control a Lung Metastasis–Specific Transcriptional Program in Breast Cancer Cells

Carmen Citterio, Mauricio Menacho-Márquez, Ramón García-Escudero, Romain M. Larive, Olga Barreiro, Francisco Sánchez-Madrid, Jesús M. Paramio, Xosé R. Bustelo*

*To whom correspondence should be addressed. E-mail: xbustelo{at}usal.es

This PDF file includes:

• Fig. S1. Human tumors show differential abundance of Rho GEF transcripts.
• Fig. S2. Abundance of Vav family mRNAs and proteins in cell lines used in this study.
• Fig. S3. Vav proteins control a large transcriptomal program in breast cancer cells.
• Fig. S4. Regulation of the breast cancer cell transcriptome by Vav proteins.
• Fig. S5. Vav proteins control the breast cancer cell transcriptome through common, synergistic, and Vav family member–specific routes.
• Fig. S6. Generation of knockdown cell lines for Vav family–dependent targets.
• Fig. S7. Vav-dependent mRNA signatures have prognostic value in breast cancer.
• Table S1. Differential abundance of Rho GEFs in human breast cancer subtypes.
• Table S2. Abundance of Vav2 and Vav3 mRNAs in the breast cancer luminal A and B subtypes.
• Table S3. Cell lines used in this study.
• Table S4. Metastasis of 4T1 knockdown cell clones in recipient mice.
  

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Other Supplementary Material for this manuscript includes the following:

• Table S5 (Microsoft Excel format). Transcriptomal changes in 4T1 cells lacking Vav2 and Vav3.
• Table S6 (Microsoft Excel format). The Vav2/Vav3-dependent transcriptome associated to the metastatic potential of the 4T1 cells used in this study.
• Table S7 (Microsoft Excel format). Overexpressed and repressed genes from table S5 associated with human cancer clinical outcome.
• Table S8 (Microsoft Excel format). Genes belonging to the Vav2/Vav3 lung metastasis signature.

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© 2012 American Association for the Advancement of Science