A dual role for Ca2+ in autophagy regulation

Decuypere, Jean-Paul; Bultynck, Geert; Parys, Jan B.

doi:10.1016/j.ceca.2011.04.001

Cited by 239 publications

(238 citation statements)

References 65 publications

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“…The IP 3 R calcium release channel of the ER is considered a key player in autophagy [60,61]. The IP 3 R is known to reside in the ER membranes within ER-mitochondria contact sites and to provide basal constitutive low-level Ca 2þ signalling to sustain mitochondrial Ca 2þ uptake required for efficient mitochondrial respiration and maintenance of normal cell bioenergetics [61].…”

Section: Ca 2þ Remodelling In Conferring Apoptosis Resistancementioning

confidence: 99%

Remodelling of Ca²⁺transport in cancer: how it contributes to cancer hallmarks?

Prevarskaya

Ouadid-Ahidouch²,

Skryma

et al. 2014

Phil. Trans. R. Soc. B

226

195

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Cancer involves defects in the mechanisms underlying cell proliferation, death and migration. Calcium ions are central to these phenomena, serving as major signalling agents with spatial localization, magnitude and temporal characteristics of calcium signals ultimately determining cell's fate. Cellular Ca 2+ signalling is determined by the concerted action of a molecular Ca 2+ -handling toolkit which includes: active energy-dependent Ca 2+ transporters, Ca 2+ -permeable ion channels, Ca 2+ -binding and storage proteins, Ca 2+ -dependent effectors. In cancer, because of mutations, aberrant expression, regulation and/or subcellular targeting of Ca 2+ -handling/transport protein(s) normal relationships among extracellular, cytosolic, endoplasmic reticulum and mitochondrial Ca 2+ concentrations or spatio-temporal patterns of Ca 2+ signalling become distorted. This causes deregulation of Ca 2+ -dependent effectors that control signalling pathways determining cell's behaviour in a way to promote pathophysiological cancer hallmarks such as enhanced proliferation, survival and invasion. Despite the progress in our understanding of Ca 2+ homeostasis remodelling in cancer cells as well as in identification of the key Ca 2+ -transport molecules promoting certain malignant phenotypes, there is still a lot of work to be done to transform fundamental findings and concepts into new Ca 2+ transport-targeting tools for cancer diagnosis and treatment.

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Section: Ca 2þ Remodelling In Conferring Apoptosis Resistancementioning

confidence: 99%

Remodelling of Ca²⁺transport in cancer: how it contributes to cancer hallmarks?

Prevarskaya

Ouadid-Ahidouch²,

Skryma

et al. 2014

Phil. Trans. R. Soc. B

226

195

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“…63 In unstressed cells a constitutive Ca 2+ release from ER to mitochondria is required for mitochondrial ATP production. A high ATP/AMP ratio inhibits AMPK and subsequently autophagy.…”

Section: Two Different Camentioning

confidence: 99%

Ins(1,4,5)P₃receptor-mediated Ca²⁺signaling and autophagy induction are interrelated

et al. 2011

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Immunoprecipitation experiments showed that during starvation Beclin 1, released from Bcl-2, first bound with increasing efficiency to Ins(1,4,5)P 3 Rs; after reaching a maximal binding after 3 h, binding, however, decreased again. The interaction site of Beclin 1 was determined to be present in the N-terminal Ins(1,4,5)P 3 -binding domain of the Ins(1,4,5) P 3 R. The starvation-induced Ins(1,4,5)P 3 R sensitization was abolished in cells treated with BECN1 siRNA, but not with ATG5 siRNA, pointing toward an essential role of Beclin 1 in this process. Moreover, recombinant Beclin 1 sensitized Ins(1,4,5) P 3 Rs in 45 Ca 2+ -flux assays, indicating a direct regulation of Ins(1,4,5)P 3 R activity by Beclin 1. Finally, we found that Ins(1,4,5) P 3 R-mediated Ca 2+ signaling was critical for starvation-induced autophagy stimulation, since the Ca 2+ chelator BAPTA-AM as well as the Ins(1,4,5)P 3 R inhibitor xestospongin B abolished the increase in LC3 lipidation and GFP-LC3-puncta formation. Hence, our results indicate a tight and essential interrelation between intracellular Ca 2+ signaling and autophagy stimulation as a proximal event in response to starvation.

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“…Subsequently, sustained Ca 2C signaling in the cytosol will result in autophagy activation through many effector molecules. 18,19 In this respect, a mechanism for activation of autophagy by inhibition of the MTOR pathway has been proposed. Ca 2C released from intracellular stores or imported from the extracellular space via distinct calcium channels activates CAMKK2/CaMKKb, which phosphorylates and activates AMPK.…”

Section: Intracellular Calcium Signaling Regulates Autophagy Via Calcmentioning

confidence: 99%

Intracellular calcium signaling regulates autophagy via calcineurin-mediated TFEB dephosphorylation

Tong

Song²

2015

Autophagy

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A dual role for Ca2+ in autophagy regulation

Cited by 239 publications

References 65 publications

Remodelling of Ca²⁺transport in cancer: how it contributes to cancer hallmarks?

Remodelling of Ca²⁺transport in cancer: how it contributes to cancer hallmarks?

Ins(1,4,5)P₃receptor-mediated Ca²⁺signaling and autophagy induction are interrelated

Intracellular calcium signaling regulates autophagy via calcineurin-mediated TFEB dephosphorylation

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A dual role for Ca2+ in autophagy regulation

Cited by 239 publications

References 65 publications

Remodelling of Ca2+transport in cancer: how it contributes to cancer hallmarks?

Remodelling of Ca2+transport in cancer: how it contributes to cancer hallmarks?

Ins(1,4,5)P3receptor-mediated Ca2+signaling and autophagy induction are interrelated

Intracellular calcium signaling regulates autophagy via calcineurin-mediated TFEB dephosphorylation

Contact Info

Product

Resources

About

Remodelling of Ca²⁺transport in cancer: how it contributes to cancer hallmarks?

Remodelling of Ca²⁺transport in cancer: how it contributes to cancer hallmarks?

Ins(1,4,5)P₃receptor-mediated Ca²⁺signaling and autophagy induction are interrelated