| Autor: |
Matthew J. Lazzara, Donald M. O'Rourke, M. Celeste Simon, Maria Martinez-Lage, Ramana V. Davuluri, Yingtao Bi, Lijoy K. Mathew, Janine M. Buonato, Gurpreet S. Kapoor, Alice M. Walsh |
| Rok vydání: |
2023 |
| DOI: |
10.1158/1541-7786.22515090.v1 |
| Popis: |
Supplementary Tables 1 and 2, Figures 1-9. Supplemental Table 1. H-score analysis for SPRY2 staining in 10 EGFRvIII-negative and 10 EGFRvIII-positive tumors. Supplemental Table 2. Upregulated genes shared by human GBMs expressing EGFRvIII and 9L.EGFRvIII rat tumors compared to wild-type EGFR human GBMs or 9L.EV rat tumors. Supplemental Figure 1. SPRY2 is efficiently knocked down by shRNA expression in GBM cell lines. Supplemental Figure 2. SPRY2 knockdown by a second non-overlapping shRNA reduces cellular proliferation, and SPRY2 knockdown by transient siRNA transfection reduces colony formation in soft agar in EGFRvIII-expressing cells. Supplemental Figure 3. SPRY2 knockdown increases cellular sensitivity to EGFR and c-MET co-inhibition. Supplemental Figure 4. SPRY2 knockdown promotes response to EGFR and c-MET coinhibition in GSC cells. Supplemental Figure 5. p38 and JNK control anchorage-independent growth and response to EGFR and c-MET co-inhibition. Supplemental Figure 6. shRNA-mediated knockdown of MKP-1 or MKP-5 reduces MKP-1 or MKP-5 mRNA level. Supplemental Figure 7. SPRY2 protein expression in kidney and cerebellum sections by immunohistochemical analysis. Supplemental Figure 8. SPRY2 correlates well with ERK phosphorylation in a panel of GBM cell lines. Supplemental Figure 9. TCGA GBM dataset analysis reveals that SPRY2 expression is associated with reduced patient survival. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
|
