Tumour transcript levels of putative invasion markers in independent glioma patient cohorts.
a
ANXA1,
b
ITGB1
c
ACTR3,
d
PDCD6IP and
e
IGFR2 levels [Human Genome U133 Plus 2.0 Arrays, cohorts
(i) and
(iii); Human Genome U133A Array, cohort
(ii)]. Expression levels generated by Oncomine are displayed as log
2-median-centred ratio
box plots comparing normal brain tissue to GBM or other less aggressive glioma tumours. Data from three cohorts
(i) Sun et al. [
67],
(ii) TCGA [
68]
(iii) Murat et al. [
69], refer to Supplementary Tables 3 and 4 for details;
n is the number of samples,
open circles represent maximum and minimum values;
error bars represent 1.5× interquartile range; *p < 0.05; **p < 0.01; ***p < 1E
− 04; ****p < 1E
− 11.
ANXA1 levels were significantly higher in GBM compared with normal brain tissues across all three datasets, with 7.3-fold (p = 1.52E
− 26), 11.7-fold (p = 2.50E
−09) and 7.5-fold (p = 5.40E
−04) increases in
(i), (ii) and
(iii), respectively.
ANXA1 levels were also significantly higher in anaplastic astrocytomas (3.3-fold, p = 6.34E
− 04), though to a lesser degree.
ITGB1 levels were significantly higher in GBM compared with normal brain tissues across all three datasets, with 1.7-fold (p = 3.94E
−07), 4.4-fold (p = 5.0E
−12) and 5.1-fold (p = 5.0E
−03) increases in
(i), (ii) and
(iii), respectively.
ACTR3 levels displayed the same trend, with higher expression levels in GBM across all three datasets, with 1.4-fold (p = 1.25E
−07), 2.9-fold (p = 6.66E
− 13) and 1.6-fold (p = 0.007) increases in
(i), (ii) and
(iii), respectively.
PDCD6IP mRNA levels were higher in GBM (1.4-fold, p = 2.25E
− 05), diffuse astrocytoma (1.3-fold, p = 0.04), and anaplastic astrocytoma (1.3-fold, p = 0.009) compared with normal brain in dataset
(i). Compared to normal brain, GBM
PDCD6IP mRNA was increased by 2.3-fold (p = 2.16E
−11) in dataset
(ii), and 2.1-fold (p = 5.90E
−04) in dataset
(iii). In dataset
(i), IGF2R was significantly higher across four glioma subtypes compared to normal brain tissues, i.e., GBM (1.5-fold, p = 4.61E
−11), diffuse astrocytoma (1.7-fold, p = 0.007), anaplastic astrocytoma (1.2-fold, p = 0.003), and oligodendroglioma (1.3-fold, p = 6.20E
−07). In dataset
(ii), IGF2R expression was higher in GBM compared to normal brain (1.6-fold increase p = 6.51E
−05) and the same trend was observed in
(iii) where
IGF2R expression was 1.4-fold higher in GBM compared with normal brain tissue (p = 1.29E
−11). f
Box plots representing
ANXA1 normalised gene expression across the TCGA GBM classical, mesenchymal, neural and proneural transcriptional subtypes.
Open circles represent maximum and minimum outlier values; error bars represent 1.5× interquartile range; (*) significant expression change relative to the classical subtype (
vs. neural, p = 0.004;
vs. proneural, p = 1.73E
− 27); (
#) significant relative to mesenchymal subtype (
vs. neural, p = 6.76E
− 05;
vs. proneural, p = 2.02E
− 31); (
§) significant relative to the neural subtype (
vs. proneural, p = 1.15E
− 12)