期刊
CELL CALCIUM
卷 70, 期 -, 页码 3-15出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2017.07.006
关键词
Calcium; Cell cycle; Checkpoints; Apoptosis; Cancer
类别
资金
- La Ligue contre le Cancer (equipe labelisee)
- Agence National de la Recherche (ANR) - Projets blancs
- ANR under the frame of E-Rare-2
- European Research Area (ERA)-Net for Research on Rare Diseases
- Association pour la recherche sur le cancer (ARC)
- Canceropole Ile-de-France
- Institut National du Cancer (INCa)
- Institut Universitaire de France
- Fondation pour la Recherche Medicale (FRM)
- European Commission (ArtForce)
- European Research Council (ERC)
- LeDucq Foundation
- LabEx Immuno-Oncology
- RHU Torino Lumiere, the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
- SIRIC Cancer Research and Personalized Medicine (CARPEM)
- Paris Alliance of Cancer Research Institutes (PACRI)
- Fondation ARC pour la recherche sur le cancer [PJA20151203519]
- Ministry of Economy and Competitivity of Spain [BFU2015-70131R]
- Asociacion Espanola Contra el Cancer (AECC)
- Fondation Philantropia
Cytosolic Ca2+ concentration levels fluctuate in an ordered manner along the cell cycle, in line with the fact that Ca2+ is involved in the regulation of cell proliferation. Cell proliferation should be an error-free process, yet is endangered by mistakes. In fact, a complex network of proteins ensures that cell cycle does not progress until the previous phase has been successfully completed. Occasionally, errors occur during the cell cycle leading to cell cycle arrest. If the error is severe, and the cell cycle checkpoints work perfectly, this results into cellular demise by activation of apoptotic or non-apoptotic cell death programs. Cancer is characterized by deregulated proliferation and resistance against cell death. Ca2+ is a central key to these phenomena as it modulates signaling pathways that control oncogenesis and cancer progression. Here, we discuss how Ca2+ participates in the exogenous and endogenous signals controlling cell proliferation, as well as in the mechanisms by which cells die if irreparable cell cycle damage occurs. Moreover, we summarize how Ca2+ homeostasis remodeling observed in cancer cells contributes to deregulated cell proliferation and resistance to cell death. Finally, we discuss the possibility to target specific components of Ca2+ signal pathways to obtain cytostatic or cytotoxic effects. (C) 2017 Elsevier Ltd. All rights reserved.
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