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Remodeling of Calcium Entry Pathways in Cancer

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Calcium Entry Pathways in Non-excitable Cells

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 898))

Abstract

Ca2+ entry pathways play important roles in control of many cellular functions, including long-term proliferation, migration and cell death. In recent years, it is becoming increasingly clear that, in some types of tumors, remodeling of Ca2+ entry pathways could contribute to cancer hallmarks such as excessive proliferation, cell migration and invasion as well as resistance to cell death or survival. In this chapter we briefly review findings related to remodeling of Ca2+ entry pathways in cancer with emphasis on the mechanisms that contribute to increased store-operated Ca2+ entry (SOCE) and store-operated currents (SOCs) in colorectal cancer cells. Finally, since SOCE appears critically involved in colon tumorogenesis, the inhibition of SOCE by aspirin and other NSAIDs and its possible contribution to colon cancer chemoprevention is reviewed.

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Acknowledgements

This work has been funded by grants from Ministerio de Economía y competitividad, Spain (BFU2012-37146) and Junta de Castilla y León, Spain [BIO/VA46/14]. DS was supported by a predoctoral fellowship from the JAE program, National Research Council (CSIC), Spain.

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  1. Instituto de Biología y Genética Molecular (IBGM), Universidad de Valladolid y Consejo Superior de Investigaciones Científicas (CSIC), C/Sanz y Forés 3, 47003, Valladolid, Spain

    Carlos Villalobos, Diego Sobradillo, Miriam Hernández-Morales & Lucía Núñez

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  1. Carlos Villalobos
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  2. Diego Sobradillo
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  3. Miriam Hernández-Morales
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  4. Lucía Núñez
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Correspondence to Carlos Villalobos .

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  1. Depto. Fisiología, University of Extremadura, Cáceres, Spain

    Juan A. Rosado

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Villalobos, C., Sobradillo, D., Hernández-Morales, M., Núñez, L. (2016). Remodeling of Calcium Entry Pathways in Cancer. In: Rosado, J. (eds) Calcium Entry Pathways in Non-excitable Cells. Advances in Experimental Medicine and Biology, vol 898. Springer, Cham. https://doi.org/10.1007/978-3-319-26974-0_19

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