Fig. 4

SPTBN1 knockdown activated ccRCC tumorigenesis through enhancing glycolysis. A RNA-seq differential expression analysis of SPTBN1-knockdown and control 786-O cells. Volcano illustrated differentially expressed genes. B Top enriched GO pathways in shSPTBN1 and shNC 786-O groups. C GSEA analysis showed Reactome Glucose Metabolism and Reactome Glycolysis pathways were significantly enriched. D, E qRT-PCR detected the expression of glycolysis-associated genes after SPTBN1 knockdown (D) or overexpression (E). F, G WB of glycolysis-associated genes after SPTBN1 knockdown (F) or SPTBN1 overexpression (G). H Lactate concentrations in RCC cells after SPTBN1 knockdown or overexpression. I Relative glucose consumption rates in RCC cells after SPTBN1 knockdown or overexpression. J ATP concentrations in RCC cells after SPTBN1 knockdown or overexpression. K SPTBN1 knockdown decreased the suppression rate of 2-DG in 786-O and Caki-1 cells. L 2-DG could partially rescue the malignant proliferation of SPTBN1-knockdown RCC cells in clonogenicity assays. (**: P < 0.05)