Figures & data
Figure 1. Scheme summarizing several pathways that control cell proliferation during glioma progression, including the recently identified position of WIP. Representative groups are shown of membrane receptors such as tyrosine kinase receptors (IGFR, GFR) or seven-transmembrane receptors (such as Wnt receptor). Through various mechanisms, these receptors can trigger generic PI3K-Akt signaling, which controls WIP activity. In many tumor cell types, certain proto-oncogenic proteins, such as the mutant versions of p53, enhance these membrane receptor activities. The oncogenic function of WIP operates by controlling YAP/TAZ stability/degradation. In some tumor cell types, YAP/TAZ can work together with beta-catenin; this collaboration enhances the relevance of this regulatory pathway, as an abundance of genes could be upregulated to ensure proliferation and survival. Levels of active GTPases such as RhoA are modified in some WIP-deficient cells, whereas in other cases Rac activity can compensate WIP-deficient function and/or WIP levels.
