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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/45054

    Título
    A reciprocal shift in transient receptor potential channel 1 (TRPC1) and stromal interaction molecule 2 (STIM2) contributes to Ca2+remodeling and cancer hallmarks in colorectal carcinoma cells
    Autor
    Sobradillo Luengo, Diego
    Hernández Morales, Miriam
    Ubierna, Daniel
    Moyer, Mary P.
    Núñez Llorente, LucíaAutoridad UVA
    Villalobos Jorge, Carlos
    Año del Documento
    2014
    Editorial
    Elsevier
    Descripción
    Producción Científica
    Documento Fuente
    Journal of Biological Chemistry, 2014, vol. 289, n. 42. p. 28765-28782
    Résumé
    We have investigated the molecular basis of intracellular Ca2+ handling in human colon carcinoma cells (HT29) versus normal human mucosa cells (NCM460) and its contribution to cancer features. We found that Ca2+ stores in colon carcinoma cells are partially depleted relative to normal cells. However, resting Ca2+ levels, agonist-induced Ca2+ increases, store-operated Ca2+ entry (SOCE), and store-operated currents (ISOC) are largely enhanced in tumor cells. Enhanced SOCE and depleted Ca2+ stores correlate with increased cell proliferation, invasion, and survival characteristic of tumor cells. Normal mucosa cells displayed small, inward Ca2+ release-activated Ca2+ currents (ICRAC) mediated by ORAI1. In contrast, colon carcinoma cells showed mixed currents composed of enhanced ICRAC plus a nonselective ISOC mediated by TRPC1. Tumor cells display increased expression of TRPC1, ORAI1, ORAI2, ORAI3, and STIM1. In contrast, STIM2 protein was nearly depleted in tumor cells. Silencing data suggest that enhanced ORAI1 and TRPC1 contribute to enhanced SOCE and differential store-operated currents in tumor cells, whereas ORAI2 and -3 are seemingly less important. In addition, STIM2 knockdown decreases SOCE and Ca2+ store content in normal cells while promoting apoptosis resistance. These data suggest that loss of STIM2 may underlie Ca2+ store depletion and apoptosis resistance in tumor cells. We conclude that a reciprocal shift in TRPC1 and STIM2 contributes to Ca2+ remodeling and tumor features in colon cancer.
    Palabras Clave
    Colorectal cancer
    Cáncer colorrectal
    Calcium
    Calcio
    ISSN
    0021-9258
    Revisión por pares
    SI
    DOI
    10.1074/jbc.M114.581678
    Patrocinador
    Ministerio de Economía, Industria y Competitividad (grants BFU2009-08967 and BFU2012-37)
    Junta de Castilla y León (grant VA145U13)
    Version del Editor
    https://www.sciencedirect.com/science/article/pii/S002192582037352X?via%3Dihub
    Propietario de los Derechos
    © 2014 Elsevier
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/45054
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
    Aparece en las colecciones
    • CFC - Artículos de Revista [38]
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    A-reciprocal-shift-in-transient.pdf
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    Attribution-NonCommercial-NoDerivs 3.0 UnportedExcepté là où spécifié autrement, la license de ce document est décrite en tant que Attribution-NonCommercial-NoDerivs 3.0 Unported

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