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Open AccessFeature PaperArticle

Highlighting Curcumin-Induced Crosstalk between Autophagy and Apoptosis as Supported by Its Specific Subcellular Localization

1
Laboratory of Cytomics, Joint Research Unit, University of Valencia, Avda. Blasco Ibanez 15, 46010 Valencia and Principe Felipe Research Center, Cerrer d’Eduardo Primo Yufera 3, 46012 Valencia, Spain
2
CNRS UMR 8003, SPPIN—Saints Pères Paris Institute for the Neurosciences, Univerity of Paris, Campus Saint-Germain, 45 rue des Saint-Pères, 75006 Paris, France
3
LVTS—Laboratory for Vascular Translational Science, UMR1148 INSERM, Université Paris XIII, Sorbonne Paris Cité, F-93017 Bobigny, France
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Division of Molecular Medicine, Ruder Boškovic Institute, Bijenička cesta 54, 10000 Zagreb, Croat
5
Université Sorbonne Paris Cité—UPMC, Paris 6, Laboratoire Jean Perrin, 75005 Paris, France
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Present address: Ludwig Institute for Cancer Research, Département d’Oncologie Fondamentale, Université de Lausanne, Chemin des Boiveresses 155, 1066 Epalinges, Switzerland.
§
Present address: Head of the Pharmacology and Toxicology Department, Faculty of Pharmacy, Albaath University, Homs 0096331, Syria.
Cells 2020, 9(2), 361; https://doi.org/10.3390/cells9020361
Received: 22 November 2019 / Revised: 8 January 2020 / Accepted: 15 January 2020 / Published: 4 February 2020
(This article belongs to the Section Cell Signaling and Regulated Cell Death)
Curcumin, a major active component of turmeric (Curcuma longa, L.), is known to have various effects on both healthy and cancerous tissues. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effect of curcumin is still unclear. Since there is a recent consensus about endoplasmic reticulum (ER) stress being involved in the cytotoxicity of natural compounds, we have investigated using Image flow cytometry the mechanistic aspects of curcumin’s destabilization of the ER, but also the status of the lysosomal compartment. Curcumin induces ER stress, thereby causing an unfolded protein response and calcium release, which destabilizes the mitochondrial compartment and induce apoptosis. These events are also associated with secondary lysosomal membrane permeabilization that occurs later together with an activation of caspase-8, mediated by cathepsins and calpains that ended in the disruption of mitochondrial homeostasis. These two pathways of different intensities and momentum converge towards an amplification of cell death. In the present study, curcumin-induced autophagy failed to rescue all cells that underwent type II cell death following initial autophagic processes. However, a small number of cells were rescued (successful autophagy) to give rise to a novel proliferation phase. View Full-Text
Keywords: apoptosis; autophagy; calcium; cancer; cell death; endoplasmic reticulum; lysosome; real-time cellular impedance; ROS; xCELLigence apoptosis; autophagy; calcium; cancer; cell death; endoplasmic reticulum; lysosome; real-time cellular impedance; ROS; xCELLigence
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Sala de Oyanguren, F.J.; Rainey, N.E.; Moustapha, A.; Saric, A.; Sureau, F.; O’Connor, J.-E.; Petit, P.X. Highlighting Curcumin-Induced Crosstalk between Autophagy and Apoptosis as Supported by Its Specific Subcellular Localization. Cells 2020, 9, 361.

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