Fig. 8

SNHG4 enhances cell resistance to enzalutamide in vitro and in vivo. a and b A dual-luciferase assay was performed to assess the interactions between let-7 miRNAs and luciferase vectors containing wild-type or mutant SNHG4 in 22Rv1 and LNCaP cells. c qRT‒PCR confirmed that overexpressing plasmids containing either wild-type or mutant SNHG4 were capable of inducing the overexpression of the SNHG4 gene in PCa cells. d and e Western blot analysis was performed to measure the expression of RRM2, EZH2, AURKA and TK1 in response to overexpression of wild-type or mutant SNHG4. f Control LNCaP cells and engineered LNCaP cells (overexpression of wild-type or mutant SNHG4) were treated with DMSO or increasing doses of enzalutamide for 24 h, and the cell survival rate was assessed by CCK-8 analysis. g The cell survival curve showed that compared to parental LNCaP cells, enzalutamide-resistant LNCaP cells demonstrated significant resistance to enzalutamide treatment; however, knockdown of SNHG4 notably weakened the enza-resistant ability. h Diagram showing the flow of animal experiments. i In vivo tumor lumps removed from four groups of CDX mice. j The tumor growth curves for in vivo tumor volumes. k The mean tumor weight of each group. i Expression of SNHG4, RRM2, EZH2, AURKA or TK1 was measured in xenograft tumors composed of control or SNHG4-overexpressing LNCaP cells by ISH/IHC staining. Magnification: 200X. m The staining intensity of each gene/protein in xenograft tumors composed of control or SNHG4-overexpressing LNCaP cells was calculated and compared. ns indicates not significant, * indicates p < 0.05, ** indicates p < 0.01