MTOR-independent autophagy induced by interrupted endoplasmic reticulum-mitochondrial Ca2 communication: a dead end in cancer cells

作者：Ahumada Castro, Ulises; Silva Pavez, Eduardo; Lovy, Alenka; Pardo, Evelyn; Molgo, Jordi; Cardenas, Cesar^*

来源：Autophagy, 2019, 15(2): 358-361.

DOI：10.1080/15548627.2018.1537769

• AMPK
• ITPRs/inositol 1
• 4
• 5-triphosphate receptors
• mitochondria associated membranes
• MCU

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.

• 出版日期2019-2-1
• 单位中国地震局