Figure 1.

Schematic representation of some elements that play a key role in the tumour-initiating cells (TICs). The Akt 1 isoform may control the viability versus apoptosis in CSCs derived from breast cancer cell lines through the control of FoxO phosphorylation. The knockdown of Akt 1 in these TICs triggered apoptosis through a mechanism FoxO3a-Bim dependent. TICs derived from gliomas, mutations of p53, correlated with high levels of WASP-interacting protein (WIP) protein and Yes-associated protein 1 (YAP)/Transcriptional co-activator with PDZ-binding motif (TAZ). In these TICs the presence of high levels of WIP are essential to maintain the proliferation and CSC-phenotype through mp53 and Akt2. Whereas, high levels of WIP control the high levels of YAP/TAZ, preventing its degradation trough proteasome. Red arrows indicated the pro-oncogenic pathways, black discontinued arrows indicated two potential stages of the same protein; red discontinued arrows indicated not necessarily direct links. Abbreviations: CSC: Cancer Stem cells; PI3K: Phosphoinositide 3-kinase Class I; Akt: viral oncogene protein kinase; Foxo 3a: Forkhead box O3; EGF: Epidermal Growth Factor; FGF: fibroblast growth factor; TEAD: Trancription factor TEA domain member 1; CTGF: Connective tissue growth factor; AREG: Amphiregulin; BIRC5 Baculoviral IAP repeat-containing protein 5; Mst 1/2: Serine/threonine-protein kinase3/4; Lats 1/2: Large tumor suppressor kinase 1/2; β-Trcp: beta-transducin repeat containing protein.