Artículos de revistas
MTOR-independent autophagy induced by interrupted endoplasmic reticulum-mitochondrial Ca2+ communication: a dead end in cancer cells
Fecha
2019Registro en:
Ahumada-Castro, U., Silva-Pavez, E., Lovy, A., Pardo, E., Molgό, J., & Cárdenas, C. (2019). MTOR-independent autophagy induced by interrupted endoplasmic reticulum-mitochondrial Ca2+ communication: a dead end in cancer cells. Autophagy, 15(2), 358-361.
1554-8627
1554-8635
DOI: 10.1080/15548627.2018.1537769
Autor
Silva-Pavez, Eduardo [Univ Mayor, Ctr Integrat Biol, Fac Sci, Santiago, Chile]
Ahumada-Castro, Ulises [Univ Mayor, Ctr Integrat Biol, Fac Sci, Santiago, Chile]
Lovy, Alenka
Pardo, Evelyn
Molgo, Jordi
Cardenas, César
Institución
Resumen
The interruption of endoplasmic reticulum (ER)-mitochondrial Ca2+ communication induces a bioenergetic crisis characterized by an increase of MTOR-independent AMPK-dependent macroautophagic/autophagic flux, which is not sufficient to reestablish the metabolic and energetic homeostasis in cancer cells. Here, we propose that upon ER-mitochondrial Ca2+ transfer inhibition, AMPK present at the mitochondria-associated membranes (MAMs) activate localized autophagy via BECN1 (beclin 1). This local response could prevent the proper interorganelle communication that would allow the autophagy-derived metabolites to reach the necessary anabolic pathways to maintain mitochondrial function and cellular homeostasis.