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:(L.T.) and (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.
Format: Adobe Acrobat PDF
Size: 2.5 MB
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-RAFV600E and AKTMyr, and GTL16 expressing K-RASG12V treated with PHA.
- Table S7. Mutational analysis of Met- and EGFR-addicted cell lines.
Format: Microsoft Excel
Size: 1.25 MB (compressed); 5.21 MB (decompressed)
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Citation: A. Bertotti, M. F. Burbridge, S. Gastaldi, F. Galimi, D. Torti, E. Medico, S. Giordano, S. Corso, G. Rolland-Valognes, B. P. Lockhart, J. A. Hickman, P. M. Comoglio, L. Trusolino, Only a Subset of Met-Activated Pathways Are Required to Sustain Oncogene Addiction. Sci. Signal. 2, ra80 (2009).