Only a Subset of Met-Activated Pathways Are Required to Sustain Oncogene Addiction

Andrea Bertotti, Mike F. Burbridge, Stefania Gastaldi, Francesco Galimi, Davide Torti, Enzo Medico, Silvia Giordano, Simona Corso, Gaëlle Rolland-Valognes, Brian P. Lockhart, John A. Hickman, Paolo M. Comoglio,* Livio Trusolino*

*To whom correspondence should be addressed. E-mail: livio.trusolino{at}ircc.it (L.T.) and paolo.comoglio{at}ircc.it (P.M.C.)

This PDF file includes:

• Fig. S1. Validation of phosphoprotein antibodies for multiplex phosphoproteomic analysis.
• Fig. S2. Met inhibition has little or no effects on the activation of p38 MAPK, JNK, STAT3, and NF-κB.
• Fig. S3. Met inhibition neutralizes the activity of AKT and ERK1/2.
• Fig. S4. Microarray validation by TaqMan low-density quantitative PCR arrays.
• Fig. S5. Effects of MEK, PI3K, and AKT inhibitors on downstream effectors in GTL16 cells.
• Fig. S6. Basal proliferation curves of PHA-resistant GTL16 cells.

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Other Supplementary Material for this manuscript includes the following:

• Table S1. Phosphoproteomic analysis of cell lines treated with PHA or gefitinib.
• Table S2. Transcriptional profiles of GTL16 and DiFi cells treated with PHA or gefitinib.
• Table S3. Functional annotation analysis of genes significantly downregulated by PHA in GTL16 cells.
  
• Table S4. Gene set enrichment analysis (GSEA) results for Genesets downregulated by PHA in GTL16 cells.
• Table S5. TaqMan validation of the transcriptional response to Met inhibition in Met-amplified cell lines.
• Table S6. Transcriptional profiles of control GTL16 (mock), GTL16 expressing B-RAF^V600E and AKT^Myr, and GTL16 expressing K-RAS^G12V treated with PHA.
• Table S7. Mutational analysis of Met- and EGFR-addicted cell lines.

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© 2009 American Association for the Advancement of Science