Figure S8 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 27K, GATA3 expression in ccRCCs</p

Figure S7 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 311K, Loss of miR-30a-3p promotes UMRC2 tumor growth</p

Figure S3 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 123K, Regulation of HIF2? by miR-30c-2-3p and miR-30a-3p in ccRCCs</p

Supplementary Data from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 162K, Methods and supplementary figure legends</p

Figure S6 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 463K, Cell survival is reduced upon increased miR-30c-2-3p expression in RCC cells</p

Figure S2 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 42K, miR-30c-2-3p and miR-30a-3p are not regulated by HIFs</p

Figure S4 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 53K, Cell proliferation modulated by miR-30c-2-3p in ccRCCs</p

Figure S5 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 28K, miR-30c-2-3p, miR-30a-3p and HIF2? levels in stable UMRC2 cells</p

Figure S1 from Restricted Expression of <i>miR-30c-2-3p</i> and <i>miR-30a-3p</i> in Clear Cell Renal Cell Carcinomas Enhances HIF2α Activity

PDF file 84K, Genomic loci and expression of miR-30c-2-3p and miR-30a-3p in ccRCCs</p

Supplementary Tables 1 and 2, Figures 1-9 from Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma

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.</p