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    J Cell Physiol. 2009 Apr;219(1):84-93.

    Oncogenic H-Ras and PI3K signaling can inhibit E-cadherin-dependent apoptosis and promote cell survival after photodynamic therapy in mouse keratinocytes.

    Espada J, Galaz S, Sanz-Rodríguez F, Blázquez-Castro A, Stockert JC, Bagazgoitia L, Jaén P, González S, Cano A, Juarranz A.

    Source

    Instituto de Investigaciones Biomédicas Alberto Sols, CSIC-Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain. jespada@iib.uam.es

    Abstract

    Maintenance of E-cadherin mediated cell-cell contacts is often required for the survival of epithelial cells and tissues. Here we report that oncogenic activation of H-Ras in murine keratinocytes can prevent cell death induced by immunological disruption of E-cadherin adhesion. A similar situation was observed in cells showing constitutive activation of the p110 alpha catalytic subunit of class IA PI3K. This protective effect is associated with beta-catenin-dependent transcription and with activation of survival factor Akt/PKB. In addition, we induced cell death by employing photodynamic therapy, using Zn-phthalocyanine as a photosensitizer that targets E-cadherin adhesion complexes. We have found that cell death based on this photodynamic action is also bypassed in cells showing constitutive activation of H-Ras and p110 alpha. Taken together, these results indicate that H-Ras/PI3K/Akt signaling plays a key role in cell survival mediated by E-cadherin cell-cell contacts.

    (c) 2008 Wiley-Liss, Inc.

    PMID:
    19065634
    [PubMed - indexed for MEDLINE]

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