Figure S1. Expression of miR-106b-93-25 cluster and host gene MCM7 in 4 molecular subgroups. Expression of (A) miR-25, (B) miR-93, (C) miR-106b, and (D) MCM7 was not associated with molecular subgroups. NanoString Technology was employed to assign molecular affiliation in MB tumours [39]. Molecular subgroup was available in 26 samples.


Figure S2. (A) Genomic aberration in medulloblastoma. Representative fluorescent in situ hybridization (FISH) findings from tumours (A) with MCM7 gain and (B) without MCM7. MCM7 was labelled in red, and the centromere 7 probe was labelled in green. (C) A positive correlation between miR-25 expression and percentage of nuclei with ≥3 signals for target locus (Spearman correlation test, P = 0.046). (DF) Tumours with higher percentage of nuclei with abnormal signals for target locus showed a trend for increasing miR-93, miR-106b, and MCM7 expression.


Figure S3. Effects of alteration of miR-25 and miR-93 expression in DAOY and ONS-76 cells. (A) DAOY and (B) ONS-76 cells were transfected with miR-25 inhibitor, miR-25, or their respective negative controls. Similarly, (C) DAOY and (D) ONS-76 cells were transfected with miR-93 inhibitor, miR-93, or their respective negative controls. Cell proliferation was studied by MTT assay at 24, 48, 72, and 96 h post transfection.


Figure S4. Effects of repression of miR-106b on (A) DNA content and expression of (B) cell cycle regulators and (C) cleaved PARP of ONS-76 cells.


Figure S5. Effects of miR-106b on (A) migration and (B) invasion of ONS-76 cells.


Figure S6. Expression of (top) Nanog, (middle) Nestin, and (bottom) SOX2 in DAOY cells grown in monolayer and tumour sphere conditions as revealed by quantitative RT-PCR.


Figure S7. Effects of miR-106b alteration in tumour sphere formation of UW228-1 cells.


Figure S8. A trend toward inverse correlation between miR-106b expression and PTEN mRNA abundance in 32 MB samples (P = 0.059).


Figure S9. Suppression of miR-106b downregulated AKT phosphorylation without affecting total AKT. DAOY and ONS-76 cells were transfected with miR-106b inhibitor or negative control. Proteins were isolated for western blot analysis for AKT and P-AKT (Ser473). Normalization was performed with GAPDH. The blots represented a typical result of three individual experiments. The numbers below the protein bands indicated the relative protein level ± SEM.


Table S1. Primer sequences for quantitative RT-PCR used in this study.


Table S2. List of 49 candidate miR-106b genes predicted by all four computational algorithms.


Table S3. PTEN expression of 32 MB samples.

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