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. 2017 Oct 6;8:797. doi: 10.1038/s41467-017-00842-8

Table 1.

The most enriched canonical pathways associated with the target genes of miRNAs modulated upon APE1-silencing

Ingenuity canonical pathways −log(P-value) Ratio
Molecular mechanisms of cancer 8.39 0.12
Chronic myeloid leukemia signaling 6.61 0.18
Cardiac hypertrophy signaling 6.36 0.13
Glioma signaling 6.22 0.17
Estrogen-mediated S-phase entry 6.20 0.38
Glioblastoma multiforme signaling 5.96 0.15
IL-8 signaling 5.87 0.13
PPARa/RXRa activation 5.63 0.14
Endothelin-1 signaling 5.25 0.13
PEDF signaling 5.22 0.18
Myc-mediated apoptosis signaling 4.80 0.19
HGF signaling 4.69 0.15
Glucocorticoid receptor signaling 4.59 0.11
Pancreatic adenocarcinoma signaling 4.55 0.14
Hepatic fibrosis/hepatic stellate cell activation 4.42 0.12
G-protein coupled receptor signaling 4.26 0.10
Role of NFAT in cardiac hypertrophy 4.11 0.12

Statistical significance and the ratio of genes included in the pathway are shown. Target genes prediction and pathway enrichment analysis were performed using IPA (see also Supplementary Data File 1). APE1 apurinic/apyrimidinic endonuclease 1, HGF hepatocyte growth factor, IPA Ingenuity Pathway Analysis, PEDF pigment epithelium-derived factor, NFAT nuclear factor of activated T cells