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• W2806857078 endingPage "191" @default.
• W2806857078 startingPage "191" @default.
• W2806857078 abstract "Wild-type p53 (wtp53) is described as a tumour suppressor gene, and mutations in p53 occur in many human cancers. Indeed, in high-grade malignant glioma, numerous molecular genetics studies have established central roles of RTK-PI3K-PTEN and ARF-MDM2-p53 INK4a-RB pathways in promoting oncogenic capacity. Deregulation of these signalling pathways, among others, drives changes in the glial/stem cell state and environment that permit autonomous growth. The initially transformed cell may undergo subsequent modifications, acquiring a more complete tumour-initiating phenotype responsible for disease advancement to stages that are more aggressive. We recently established that the oncogenic activity of mutant p53 (mtp53) is driven by the actin cytoskeleton-associated protein WIP (WASP-interacting protein), correlated with tumour growth, and more importantly that both proteins are responsible for the tumour-initiating cell phenotype. We reported that WIP knockdown in mtp53-expressing glioblastoma greatly reduced proliferation and growth capacity of cancer stem cell (CSC)-like cells and decreased CSC-like markers, such as hyaluronic acid receptor (CD44), prominin-1 (CD133), yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ). We thus propose a new CSC signalling pathway downstream of mtp53 in which Akt regulates WIP and controls YAP/TAZ stability. WIP drives a mechanism that stimulates growth signals, promoting YAP/TAZ and β-catenin stability in a Hippo-independent fashion, which allows cells to coordinate processes such as proliferation, stemness and invasiveness, which are key factors in cancer progression. Based on this multistep tumourigenic model, it is tantalizing to propose that WIP inhibitors may be applied as an effective anti-cancer therapy." @default.
• W2806857078 created "2018-06-13" @default.
• W2806857078 creator A5033868474 @default.
• W2806857078 creator A5043034701 @default.
• W2806857078 creator A5084027100 @default.
• W2806857078 date "2018-06-09" @default.
• W2806857078 modified "2023-10-16" @default.
• W2806857078 title "WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma" @default.
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• W2806857078 doi "https://doi.org/10.3390/cancers10060191" @default.
• W2806857078 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6024887" @default.
• W2806857078 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29890731" @default.
• W2806857078 hasPublicationYear "2018" @default.
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