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Article ; Online: Assessment of Mitochondrial Cell Metabolism by Respiratory Chain Electron Flow Assays.

Radogna, Flavia / Gérard, Déborah / Dicato, Mario / Diederich, Marc

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2276, Page(s) 129–141

Abstract: Cellular energy metabolism is regulated by complex metabolic pathways. Although anaerobic glycolysis was reported as a primary source of energy in cancer leading to a high rate of lactate production, current evidence shows that the main energy source ... ...

Abstract	Cellular energy metabolism is regulated by complex metabolic pathways. Although anaerobic glycolysis was reported as a primary source of energy in cancer leading to a high rate of lactate production, current evidence shows that the main energy source supporting cancer cell metabolism relies on mitochondrial metabolism. Mitochondria are the key organelle maintaining optimal cellular energy levels. MitoPlate™ S-1 provides a highly reproducible bioenergetics tool to analyze the electron flow rate in live cells. Measuring the rates of electron flow into and through the electron transport chain using different NADH and FADH
MeSH term(s)	Cell Line, Tumor ; Electron Transport ; High-Throughput Screening Assays/methods ; Humans ; Metabolic Networks and Pathways ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Oxidation-Reduction
Language	English
Publishing date	2021-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1266-8_9
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Article ; Online: Stress-induced cellular responses in immunogenic cell death: Implications for cancer immunotherapy.

Radogna, Flavia / Diederich, Marc

Biochemical pharmacology

2018 Volume 153, Page(s) 12–23

Abstract: Cancer is evading the host's defense mechanisms leading to avoidance of immune destruction. During tumor progression, immune-evading cancer cells arise due to selective pressure from the hypoxic and nutrient-deprived microenvironment. Thus, therapies ... ...

Abstract	Cancer is evading the host's defense mechanisms leading to avoidance of immune destruction. During tumor progression, immune-evading cancer cells arise due to selective pressure from the hypoxic and nutrient-deprived microenvironment. Thus, therapies aiming at re-establishing immune destruction of pathological cells constitute innovating anti-cancer strategies. Accumulating evidence suggests that selected conventional chemotherapeutic drugs increase the immunogenicity of stressed and dying cancer cells by triggering a form of cell death called immunogenic cell death (ICD), which is characterized by the release of danger-associated molecular patterns (DAMPs). In this review, we summarize the effects of ICD inducers on DAMP signaling leading to adjuvanticity and antigenicity. We will discuss the associated stress response pathways that cause the release of DAMPs leading to improved immune recognition and their relevance in cancer immunotherapy. Our aim is to highlight the contribution of adaptive immunity to the long-term clinical benefits of anticancer treatments and the properties of immune memory that can protect cancer patients against relapse.
MeSH term(s)	Animals ; Cell Death/drug effects ; Cell Death/immunology ; Endoplasmic Reticulum Stress/drug effects ; Endoplasmic Reticulum Stress/immunology ; Humans ; Immunity, Cellular/drug effects ; Immunity, Cellular/immunology ; Immunogenetic Phenomena/drug effects ; Immunogenetic Phenomena/physiology ; Immunotherapy/methods ; Neoplasms/immunology ; Neoplasms/therapy ; Signal Transduction/drug effects ; Signal Transduction/immunology ; Stress, Physiological/drug effects ; Stress, Physiological/immunology
Language	English
Publishing date	2018-02-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2018.02.006
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Article ; Online: Natural modulators of the hallmarks of immunogenic cell death.

Radogna, Flavia / Dicato, Mario / Diederich, Marc

Biochemical pharmacology

2019 Volume 162, Page(s) 55–70

Abstract: Natural compounds act as immunoadjuvants as their therapeutic effects trigger cancer stress response and release of damage-associated molecular patterns (DAMPs). These reactions occur through an increase in the immunogenicity of cancer cells that undergo ...

Abstract	Natural compounds act as immunoadjuvants as their therapeutic effects trigger cancer stress response and release of damage-associated molecular patterns (DAMPs). These reactions occur through an increase in the immunogenicity of cancer cells that undergo stress followed by immunogenic cell death (ICD). These processes result in a chemotherapeutic response with a potent immune-mediating reaction. Natural compounds that induce ICD may function as an interesting approach in converting cancer into its own vaccine. However, multiple parameters determine whether a compound can act as an ICD inducer, including the nature of the inducer, the premortem stress pathways, the cell death pathways, the intrinsic antigenicity of the cell, and the potency and availability of an immune cell response. Thus, the identification of hallmarks of ICD is important in determining the prognostic biomarkers for new therapeutic approaches and combination treatments.
MeSH term(s)	Animals ; Antineoplastic Agents, Phytogenic/chemistry ; Antineoplastic Agents, Phytogenic/pharmacology ; Antineoplastic Agents, Phytogenic/therapeutic use ; Endoplasmic Reticulum Stress/drug effects ; Endoplasmic Reticulum Stress/immunology ; Humans ; Immunity, Cellular/drug effects ; Immunity, Cellular/immunology ; Immunogenic Cell Death/drug effects ; Immunogenic Cell Death/physiology ; Immunotherapy/methods ; Immunotherapy/trends ; Neoplasms/drug therapy ; Neoplasms/immunology
Chemical Substances	Antineoplastic Agents, Phytogenic
Language	English
Publishing date	2019-01-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2018.12.016
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Article ; Online: Cancer-type-specific crosstalk between autophagy, necroptosis and apoptosis as a pharmacological target.

Radogna, Flavia / Dicato, Mario / Diederich, Marc

Biochemical pharmacology

2015 Volume 94, Issue 1, Page(s) 1–11

Abstract: Cell death plays an essential role in the development of organs, homeostasis, and cancer. Apoptosis and programmed necrosis are two major types of cell death, characterized by different cell morphology and pathways. Accumulating evidence shows autophagy ... ...

Abstract	Cell death plays an essential role in the development of organs, homeostasis, and cancer. Apoptosis and programmed necrosis are two major types of cell death, characterized by different cell morphology and pathways. Accumulating evidence shows autophagy as a new alternative target to treat tumor resistance. Besides its well-known pro-survival role, autophagy can be a physiological cell death process linking apoptosis and programmed necrosis cell death pathways, by various molecular mediators. Here, we summarize the effects of pharmacologically active compounds as modulators of different types of cancer cell death depending on the cellular context. Indeed, current findings show that both natural and synthetic compounds regulate the interplay between apoptosis, autophagy and necroptosis stimulating common molecular mediators and sharing common organelles. In response to specific stimuli, the same death signal can cause cells to switch from one cell death modality to another depending on the cellular setting. The discovery of important interconnections between the different cell death mediators and signaling pathways, regulated by pharmacologically active compounds, presents novel opportunities for the targeted treatment of cancer. The aim of this review is to highlight the potential role of these compounds for context-specific anticancer therapy.
MeSH term(s)	Antineoplastic Agents, Phytogenic/therapeutic use ; Apoptosis/drug effects ; Apoptosis/genetics ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Autophagy/drug effects ; Autophagy/genetics ; Beclin-1 ; Gene Expression Regulation, Neoplastic ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Necrosis/genetics ; Necrosis/metabolism ; Necrosis/pathology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Organ Specificity ; Precision Medicine ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Antineoplastic Agents, Phytogenic ; Apoptosis Regulatory Proteins ; BECN1 protein, human ; Beclin-1 ; Membrane Proteins ; Proto-Oncogene Proteins c-bcl-2 ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2015-03-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2014.12.018
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Article ; Online: Effects of Natural Products on Mcl-1 Expression and Function.

Muller, Florian / Cerella, Claudia / Radogna, Flavia / Dicato, Mario / Diederich, Marc

Current medicinal chemistry

2015 Volume 22, Issue 30, Page(s) 3447–3461

Abstract: Cancer development is mostly due to a deregulation of cell death as cancer cells become resistant to apoptosis by increasing expression of anti-apoptotic proteins belonging to the Bcl-2 family. Mcl-1 is one anti-apoptotic protein, which is mainly ... ...

Abstract	Cancer development is mostly due to a deregulation of cell death as cancer cells become resistant to apoptosis by increasing expression of anti-apoptotic proteins belonging to the Bcl-2 family. Mcl-1 is one anti-apoptotic protein, which is mainly responsible for cancer cell resistance as it is overexpressed by most cancer cell types. Many research projects aim to restore cancer cell death by using natural pharmacological scaffolds targeting anti-apoptotic proteins to inhibit their effect in cancer development. This review introduces natural compound inhibitors of the Bcl-2 protein family with a focus on Mcl-1.
MeSH term(s)	Biological Products/pharmacology ; Cardenolides/chemistry ; Cardenolides/pharmacology ; Drug Delivery Systems ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Molecular Structure ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Neoplasms/drug therapy ; Proto-Oncogene Proteins c-bcl-2/metabolism
Chemical Substances	Biological Products ; Cardenolides ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2 ; UNBS 1450
Language	English
Publishing date	2015-07-15
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1319315-6
ISSN	1875-533X ; 0929-8673
ISSN (online)	1875-533X
ISSN	0929-8673
DOI	10.2174/0929867322666150716115435
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Article: Natural compounds as regulators of the cancer cell metabolism.

Cerella, Claudia / Radogna, Flavia / Dicato, Mario / Diederich, Marc

International journal of cell biology

2013 Volume 2013, Page(s) 639401

Abstract: Even though altered metabolism is an "old" physiological mechanism, only recently its targeting became a therapeutically interesting strategy and by now it is considered an emerging hallmark of cancer. Nevertheless, a very poor number of compounds are ... ...

Abstract	Even though altered metabolism is an "old" physiological mechanism, only recently its targeting became a therapeutically interesting strategy and by now it is considered an emerging hallmark of cancer. Nevertheless, a very poor number of compounds are under investigation as potential modulators of cell metabolism. Candidate agents should display selectivity of action towards cancer cells without side effects. This ideal favorable profile would perfectly overlap the requisites of new anticancer therapies and chemopreventive strategies as well. Nature represents a still largely unexplored source of bioactive molecules with a therapeutic potential. Many of these compounds have already been characterized for their multiple anticancer activities. Many of them are absorbed with the diet and therefore possess a known profile in terms of tolerability and bioavailability compared to newly synthetized chemical compounds. The discovery of important cross-talks between mediators of the most therapeutically targeted aberrancies in cancer (i.e., cell proliferation, survival, and migration) and the metabolic machinery allows to predict the possibility that many anticancer activities ascribed to a number of natural compounds may be due, in part, to their ability of modulating metabolic pathways. In this review, we attempt an overview of what is currently known about the potential of natural compounds as modulators of cancer cell metabolism.
Language	English
Publishing date	2013-05-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2536742-0
ISSN	1687-8884 ; 1687-8876
ISSN (online)	1687-8884
ISSN	1687-8876
DOI	10.1155/2013/639401
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Article ; Online: Melatonin: a pleiotropic molecule regulating inflammation.

Radogna, Flavia / Diederich, Marc / Ghibelli, Lina

Biochemical pharmacology

2010 Volume 80, Issue 12, Page(s) 1844–1852

Abstract: Melatonin is a neurohormone produced by the pineal gland that regulates sleep and circadian functions. Melatonin also regulates inflammatory and immune processes acting as both an activator and inhibitor of these responses. Melatonin demonstrates ... ...

Abstract	Melatonin is a neurohormone produced by the pineal gland that regulates sleep and circadian functions. Melatonin also regulates inflammatory and immune processes acting as both an activator and inhibitor of these responses. Melatonin demonstrates endocrine, but also paracrine and autocrine effects in the leukocyte compartment: on one side, leukocytes respond to melatonin in a circadian fashion; on the other side, leukocytes are able to synthesize melatonin by themselves. With its endocrine and paracrine effects, melatonin differentially modulates pro-inflammatory enzymes, controls production of inflammatory mediators such as cytokines and leukotrienes and regulates the lifespan of leukocytes by interfering with apoptotic processes. Moreover, its potent antioxidant ability allows scavenging of oxidative stress in the inflamed tissues. The interesting timing of pro- and anti-inflammatory effects, such as those affecting lipoxygenase activity, suggests that melatonin might promote early phases of inflammation on one hand and contribute to its attenuation on the other hand, in order to avoid complications of chronic inflammation. This review aims at giving a comprehensive overview of the various inflammatory pathways regulated by this pleiotropic hormone.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Antioxidants/pharmacology ; Apoptosis ; Arachidonic Acid/metabolism ; Cell Survival ; Humans ; Inflammation/metabolism ; Leukocytes/cytology ; Leukocytes/physiology ; Melatonin/biosynthesis ; Melatonin/pharmacology ; Melatonin/physiology ; Oxidative Stress ; Pineal Gland/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Anti-Inflammatory Agents ; Antioxidants ; Reactive Oxygen Species ; Arachidonic Acid (27YG812J1I) ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2010-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2010.07.041
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Article ; Online: Neuroprotection by melatonin on astrocytoma cell death.

Radogna, Flavia / Nuccitelli, Silvia / Mengoni, Fabio / Ghibelli, Lina

Annals of the New York Academy of Sciences

2009 Volume 1171, Page(s) 509–513

Abstract: Glial cells play an active role in the homeostatic regulation of the central nervous system (CNS). Astrocytes, the most abundant glial cell types in the brain, provide mechanical and metabolic support for neurons. The regulation of astrocyte apoptosis, ... ...

Abstract	Glial cells play an active role in the homeostatic regulation of the central nervous system (CNS). Astrocytes, the most abundant glial cell types in the brain, provide mechanical and metabolic support for neurons. The regulation of astrocyte apoptosis, therefore, is important for physiological and pathological processes in the CNS. Melatonin is a neurohormone that regulates target cells via binding to specific high-affinity plasma membrane receptors, MT1/MT2. In addition to regulating circadian rhythms, melatonin has recently attracted much interest for its potential regulation of cell apoptosis. We recently showed that melatonin antagonizes apoptosis on U937 cells via intersecting signal transduction events involving binding to MT1/MT2 and activation of lipoxygenase. Here we describe the neuroprotective potential of melatonin, showing that melatonin significantly reduces damage-induced apoptosis in astrocytoma cells. The mechanism of protection is different from that shown in U937 cells, because it does not involve MT1/MT2 or lipoxygenase; likewise, Ca(2+) influx is not involved. Intriguingly, inhibition of phospholipase C (PLC) with neomycin reverses melatonin protection, suggesting that a PLC-dependent signal transduction, different from that triggered by MT1/MT2, is involved in the antiapoptotic pathway of melatonin.
MeSH term(s)	Antioxidants/pharmacology ; Apoptosis/drug effects ; Astrocytoma/metabolism ; Astrocytoma/pathology ; Benzoquinones/pharmacology ; Biological Transport/drug effects ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Humans ; Lipoxygenase Inhibitors/pharmacology ; Melatonin/pharmacology ; Neomycin/pharmacology ; Neuroprotective Agents/pharmacology ; Nifedipine/pharmacology ; Protein Synthesis Inhibitors/pharmacology ; Receptors, Melatonin/antagonists & inhibitors ; Tryptamines/pharmacology ; Type C Phospholipases/antagonists & inhibitors ; Type C Phospholipases/metabolism
Chemical Substances	Antioxidants ; Benzoquinones ; Calcium Channel Blockers ; Lipoxygenase Inhibitors ; Neuroprotective Agents ; Protein Synthesis Inhibitors ; Receptors, Melatonin ; Tryptamines ; luzindole (117946-91-5) ; Neomycin (1404-04-2) ; 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (80809-81-0) ; Type C Phospholipases (EC 3.1.4.-) ; Nifedipine (I9ZF7L6G2L) ; Melatonin (JL5DK93RCL) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2009-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2009.04900.x
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Article ; Online: From nature to bedside: pro-survival and cell death mechanisms as therapeutic targets in cancer treatment.

Cerella, Claudia / Teiten, Marie-Hélène / Radogna, Flavia / Dicato, Mario / Diederich, Marc

Biotechnology advances

2014 Volume 32, Issue 6, Page(s) 1111–1122

Abstract: Cell death is an important physiological regulator during development, tissue homeostasis and stress response but it is also a protective tumor suppressive mechanism. Tumor cells almost universally acquire the ability to evade cell death pathways that in ...

Abstract	Cell death is an important physiological regulator during development, tissue homeostasis and stress response but it is also a protective tumor suppressive mechanism. Tumor cells almost universally acquire the ability to evade cell death pathways that in normal cells act as a protective mechanism to remove damaged cells. As a result, a population of death-resistant cells with accumulating genetic and epigenetic abnormalities contributes to malignant transformation. Any alteration of the homeostatic balance between survival and death is therefore a critical factor in carcinogenesis. Several forms of cell death exist and cross talk among them is emerging; however, we still miss many molecular details. It becomes essential to revisit the role of each type of cell death to understand interconnections existing between different cell death pathways as well as the network of their mediators to eventually develop new effective strategies to kill cancer cells. More specifically, new therapies based on compounds selectively triggering apoptosis, necrosis or autophagy recently became both appealing and challenging. Despite the rather clear classification of the different cell death modalities according to morphological criteria and the attempt to describe them with distinct signaling pathways, the reality reveals a complex interplay between apoptosis, regulated necrosis and autophagy involving a heterogeneous mix of molecular mediators. Nature, presenting an almost endless plenitude of bioactive scaffolds, can efficiently contribute compounds that allow deciphering the intricate pathways of cell death pathways and thus eventually contribute to selectively target cancer-type specific pathways in an attempt to personalize cancer patient treatment depending on cancer death pathway specificities. The aim of this review is to provide first an overview of molecular cell death specificities and to highlight how compounds of natural origins, with or without hemisynthetic modifications, target unique thanatotic molecular constellations.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Death/drug effects ; Cell Death/physiology ; Cell Line, Tumor ; Drug Discovery ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Reactive Oxygen Species ; Signal Transduction
Chemical Substances	Antineoplastic Agents ; Reactive Oxygen Species
Language	English
Publishing date	2014-11-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	47165-3
ISSN	1873-1899 ; 0734-9750
ISSN (online)	1873-1899
ISSN	0734-9750
DOI	10.1016/j.biotechadv.2014.03.006
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Article ; Online: Tubulin-binding anticancer polysulfides induce cell death via mitotic arrest and autophagic interference in colorectal cancer.

Yagdi Efe, Esma / Mazumder, Aloran / Lee, Jin-Young / Gaigneaux, Anthoula / Radogna, Flavia / Nasim, Muhammad Jawad / Christov, Christo / Jacob, Claus / Kim, Kyu-Won / Dicato, Mario / Chaimbault, Patrick / Cerella, Claudia / Diederich, Marc

Cancer letters

2017 Volume 410, Page(s) 139–157

Abstract: Polysulfanes show chemopreventive effects against gastrointestinal tumors. We identified diallyl tetrasulfide and its derivative, dibenzyl tetrasulfide (DBTTS), to be mitotic inhibitors and apoptosis inducers. Here, we translate their application in ... ...

Abstract	Polysulfanes show chemopreventive effects against gastrointestinal tumors. We identified diallyl tetrasulfide and its derivative, dibenzyl tetrasulfide (DBTTS), to be mitotic inhibitors and apoptosis inducers. Here, we translate their application in colorectal cancer (CRC). MALDI-TOF-MS analysis identified both compounds as reversible tubulin binders, validated by in cellulo α-tubulin degradation. BRAF(V600E)-mutated HT-29 cells were resistant to DBTTS, as evidenced by mitotic arrest for 48 h prior to apoptosis induction compared to KRAS(G12V)-mutated SW480/620 cells, which committed to death earlier. The prolonged mitotic block correlated with autophagy impairment and p62 protein accumulation in HT-29 but not in SW480/620 cells, whereas siRNA-mediated p62 inhibition sensitized HT-29 cells to death. In silico analysis with 484 colorectal cancer patients associated higher p62 expression and reduced autophagic flux with greater overall survival. Accordingly, we hypothesized that DBTTS targets CRC survival/death through autophagy interference in cell types with differential autophagic capacities. We confirmed the therapeutic potential of DBTTS by the inhibition of spheroid and colony formation capacities in CRC cells, as well as in HT-29 zebrafish xenografts in vivo.
Language	English
Publishing date	2017-12-01
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2017.09.011
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