Fig. 4

Down-regulated or mutated SPOP promotes DLBCL maliganant aggressiveness depending on CHAF1A. A The violin plot exhibited the differential expression levels of SPOP between DLBCL and normal tissues based on the GSE83632 data set. B Kaplan–Meier (K–M) survival curves analysis also showed that low SPOP levels may appear to correlate with shorter OS months of DLBCL patients based on the GSE83632 data set. C The CCK8 assays in three DLBCL cell lines (DB, U2932, FARAGE) revealed that WT SPOP, but not the δBTB mutant, could suppress cell proliferation, but simultaneous overexpression of CHAF1A could partially rescue the impaired cell growth ability. D Proliferation ability of OCI-Ly7 cells was enhanced by SPOP depletion, which could be partailly impaired by CHAF1A KD. E Similarly, SPOP depletion could enhance migration of OCI-Ly7 cells, which could be partially suppressed by CHAF1A KD. F Tumor volumes curves of FARAGE-derived tumor models showed that WT SPOP, but not the δBTB mutant, could suppress in vivo tumor growth, whereas tumor-associated SPOP F102I mutant could enhance in vivo tumor growth. G The OCI-Ly7-derived tumor models showed that SPOP depletion could enhance tumor in vivo growth, which could be partially suppressed by CHAF1A KD. Tumor graph was shown on the left; Quantification of tumor volumes was shown on the middle panel; Tumor weight was compared and shown on the right panel. Experiments were performed in triplicate. *p < 0.05, **p < 0.01, ***p < 0.001