Fig. 8: AVIL regulates LIN28B expression through FOXM1.

a LIN28B was reduced upon AVIL silencing, and induced upon AVIL overexpression. U87 cells were transfected with siAVIL or siCT, and empty vector control (CT) or AVIL expressing vector. LIN28B level was measured by qRT-PCR, and normalized to that of GAPDH, and then to siCT. b LIN28B mediates at least some of the AVIL effect. U87 cells transfected with siAVIL or siCT were further transfected with LIN28B expression vector, or control plasmid (CT). Cell proliferation was measured by cell counting. Cell motility was measured by wound-healing assay. c Headpiece mutants are not as effective as WT in inducing LIN28B expression. LIN28B expression was measured by qRT-PCR and is represented relative to GAPDH levels. d Clinical correlation between the expression of LIN28B and patient survival. A two-class model, stratified by LIN28B expression using TCGA GBM data. The LIN28B high group has a significantly worse survival (p < 0.01, two-sided log-rank test). e With TCGA lower-grade glioma data, LIN28B high group is found to have worse overall survival (p = 0.00013) (two-sided log-rank test). f Let-7 family members were induced upon AVIL silencing, and suppressed upon AVIL overexpression. Let-7 family members that are expressed in U87 were measured by qRT-PCR. Their expression levels were plotted against that of siCT, or CT. *p < 0.05, **p < 0.01, ***p < 0.001. Data are presented as mean values ± SD in a–c, and f.