Supplementary Data from Extracellular Vesicle-Mediated Transfer of LncRNA IGFL2-AS1 Confers Sunitinib Resistance in Renal Cell Carcinoma

Supplementary Figure S1-S10, supplementary table S1-S8, supplementary methods. Figure S1. The construction of sunitinib-resistant model and validation of sunitinib resistance. Figure S2. Screening and identification of lncRNA IGFL2-AS1 related to sunitinib resistance. Figure S3. IGFL2-AS1 promotes sunitinib resistance of RCC cells in vitro and in vivo. Figure S4. IGFL2-AS1 overexpression enhances autophagy in RCC cells by regulating alternative splicing of TP53INP2. Figure S5. IGFL2-AS1 functions by binding to hnRNPC protein. Figure S6. IGFL2-AS1 regulates alternative splicing of TP53INP2 through competitively binding to hnRNPC. Figure S7. hnRNPC mediates IGFL2-AS1 packaging into EVs and transmission of sunitinib resistance. Figure S8. m6A epigenetic modification is critical to IGFL2-AS1 interaction with hnRNPC. Figure S9. Characteristics of C-SLN nanoparticles and in vivo application of C-SLN/ASO-IGFL2-AS1 complexes. Figure S10. Extended applicability of IGFL2-AS1 to resistance of cabozantinib and axitinib. Supplementary Table S1. Correlations between IGFL2-AS1 tissue expressions and clinical characteristics of 72 ccRCC patients in the SYSU Cohort. Supplementary Table S2. Univariate and multivariate cox regression analysis of variables associated with PFS in the SYSU cohort. Supplementary Table S3. Correlations between IGFL2-AS1 expressions in serum-derived EVs and clinical characteristics of 60 ccRCC patients in the SYSU Cohort. Supplementary Table S4. Uivariate and multivariate cox regression analysis of variables associated with PFS in the SYSU cohort. Supplementary Table S5. Clinical characteristics of RCC patients in the PDX models. Supplementary Table S6. Targeting sequence of siRNA and ASO. Supplementary Table S7. Primers used in this study for qRT-PCR analysis. Supplementary Table S8. Primary antibodies applied in this study.