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Rivas S, Antón IM, Wandosell F. WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma. Cancers (Basel). 2018;10(6)doi: 10.3390/cancers10060191.
Rivas, S., Antón, I. M., & Wandosell, F. (2018). WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma. Cancers, 10(6), . https://doi.org/10.3390/cancers10060191
Rivas, Sergio, et al. "WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma." Cancers vol. 10,6 (2018). doi: https://doi.org/10.3390/cancers10060191
Rivas S, Antón IM, Wandosell F. WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma. Cancers (Basel). 2018 Jun 09;10(6). doi: 10.3390/cancers10060191. PMID: 29890731; PMCID: PMC6024887.
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Cancers (Basel). 2018 Jun 09;10(6). doi: 10.3390/cancers10060191.

WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma.

Cancers

Sergio Rivas, Inés M Antón, Francisco Wandosell

Affiliations

  1. Centro Nacional de Biotecnología (CNB-CSIC), Darwin 3, 28049 Madrid, Spain. [email protected].
  2. Centro Nacional de Biotecnología (CNB-CSIC), 28031 Madrid, Spain. [email protected].
  3. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Nicolás Cabrera 1, 28049 Madrid, Spain. [email protected].
  4. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo 5, 28031 Madrid, Spain. [email protected].
  5. Centro Nacional de Biotecnología (CNB-CSIC), Darwin 3, 28049 Madrid, Spain. [email protected].
  6. Centro Nacional de Biotecnología (CNB-CSIC), 28031 Madrid, Spain. [email protected].
  7. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo 5, 28031 Madrid, Spain. [email protected].
  8. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Nicolás Cabrera 1, 28049 Madrid, Spain. [email protected].
  9. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo 5, 28031 Madrid, Spain. [email protected].

PMID: 29890731 PMCID: PMC6024887 DOI: 10.3390/cancers10060191

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.

Keywords: Akt; CSCs; TICs; WIP; YAP/TAZ; glioma; proliferation; signalling in cancer; survival

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