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. 2014 Sep 4;9(9):e106801. doi: 10.1371/journal.pone.0106801

Figure 8. A hypothetical regulation model of metabolic and signaling control in highly malignant STS.

Figure 8

(A) Signaling pathways, excluding cell cycle and DNA repair. (B) Cell cycle and DNA repair pathways. The pink oval indicates the genes selected in the present study. MUFA, monounsaturated fatty acid; SFA, saturated fatty acid; SCD1, stearoyl-CoA desaturase 1; MIF, macrophage migration inhibitory factor; CXCR, CXC chemokine receptor; PI3K, phosphoinositide 3-kinase; MAPK, extracellular signal-regulated kinase; ERK, mitogen-activated protein kinase; PTTG1, pituitary tumor-transforming 1; ASPM, abnormal spindle-like microcephaly-associated protein; CDC20, cell division cycle protein 20; KIF20A, kinesin family member 20A; ENO1, enolase 1; P4HA, prolyl 4-hydroxylase subunit α; PRDX1, peroxiredoxin 1; FAM162A, family with sequence similarity 162, member A; STAT1, signal transducer and activator of transcription 1; CDK1, cyclin-dependent kinase 1; TACC3, transforming, acidic coiled-coil containing protein 3; PRKDC, protein kinase, DNA-activated, catalytic polypeptide; H2AFY, H2A histone family, member Y; SLC16A1, solute carrier family 16, member 1; VEGF, vascular endothelial growth factor; HIF, hypoxia inducible factor; PLOD2, procollagen-lysine,2-oxoglutarate 5-dioxygenase 2; NF-κB, nuclear factor-kappa B.