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The ER-mitochondria Ca2+ signaling in cancer progression: Fueling the monster.
Bustos, Galdo; Ahumada-Castro, Ulises; Silva-Pavez, Eduardo; Puebla, Andrea; Lovy, Alenka; Cesar Cardenas, J.
Afiliação
  • Bustos G; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile.
  • Ahumada-Castro U; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile.
  • Silva-Pavez E; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile.
  • Puebla A; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile.
  • Lovy A; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile; Department of Neuroscience, Center for Neuroscience Research, Tufts School of Medicine, Boston, MA, United States. Electronic address: alenka.
  • Cesar Cardenas J; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile; Buck Institute for Research on Aging, Novato, CA, United States; Department of Chemistry and Biochemistry, University of California, Santa Bar
Int Rev Cell Mol Biol ; 363: 49-121, 2021.
Article em En | MEDLINE | ID: mdl-34392932
Cancer is a leading cause of death worldwide. All major tumor suppressors and oncogenes are now recognized to have fundamental connections with metabolic pathways. A hallmark feature of cancer cells is a reprogramming of their metabolism even when nutrients are available. Increasing evidence indicates that most cancer cells rely on mitochondrial metabolism to sustain their energetic and biosynthetic demands. Mitochondria are functionally and physically coupled to the endoplasmic reticulum (ER), the major calcium (Ca2+) storage organelle in mammalian cells, through special domains known as mitochondria-ER contact sites (MERCS). In this domain, the release of Ca2+ from the ER is mainly regulated by inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs), a family of Ca2+ release channels activated by the ligand IP3. IP3R mediated Ca2+ release is transferred to mitochondria through the mitochondrial Ca2+ uniporter (MCU). Once in the mitochondrial matrix, Ca2+ activates several proteins that stimulate mitochondrial performance. The role of IP3R and MCU in cancer, as well as the other proteins that enable the Ca2+ communication between these two organelles is just beginning to be understood. Here, we describe the function of the main players of the ER mitochondrial Ca2+ communication and discuss how this particular signal may contribute to the rise and development of cancer traits.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Cálcio / Retículo Endoplasmático / Mitocôndrias / Neoplasias Limite: Animals / Humans Idioma: En Revista: Int Rev Cell Mol Biol Assunto da revista: BIOLOGIA MOLECULAR Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Chile País de publicação: Holanda
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Cálcio / Retículo Endoplasmático / Mitocôndrias / Neoplasias Limite: Animals / Humans Idioma: En Revista: Int Rev Cell Mol Biol Assunto da revista: BIOLOGIA MOLECULAR Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Chile País de publicação: Holanda