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Mitochondrial Functions, Alterations and Dynamics in Cancer
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Mitochondrial Functions, Alterations and Dynamics in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (15 February 2021) | Viewed by 55049

Special Issue Editors

Dr. Monica Montopoli

E-Mail Website
Guest Editor
Department of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy
Interests: chemoresistance; cancer metabolism; chemosensitizers; cisplatin; mitochondria; molecular pharmacology; antioxidants; inflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Pierre Sonveaux

E-Mail Website
Co-Guest Editor
Pole of Pharmacology and Therapeutics, Institute of Experimental and Clinical Research, Université catholique de Louvain (UCLouvain), 1200 Brussels, Belgium
Interests: tumor metabolism; hypoxia; angiogenesis; metastasis; chemoresistance; radioresistance; glycolysis; oxidative phosphorylation; lactate; mitochondrial reactive oxygen species (mtROS); translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer cells are metabolic entities presenting a wide pattern of metabolic alterations. At the core of metabolic pathways, mitochondria are subcellular organelles specialized in energy production and biosynthesis. In the process of anaplerosis, they are fueled by several metabolic pathways (e.g., glycolysis, glutaminolysis, and fatty acid oxidation), while for cataplerosis they provide metabolites and cofactors for fatty acid and protein synthesis and resistance to redox stress. As dynamic organelles, mitochondria also control cell survival and death. As metabolic sensors, they signal through the activation of molecular pathways that affect the cell as a whole, supporting phenotypes that characterize things such as cancer-initiating cells, cancer stem cells, metastatic progenitor cells, and cancer cells resistant to therapy. Mitochondrial processes are thus harnessed and/or altered by cancer cells and contribute to the malignant phenotype, which is the topic of this Special Issue of the International Journal of Molecular Sciences. A special focus will be set on original strategies targeting mitochondria for anticancer treatment.

Prof. Monica Montopoli
Prof. Pierre Sonveaux
Guest Editors

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Keywords

  • tumor metabolism
  • mitochondria
  • anaplerosis
  • cataplerosis
  • energy production
  • biosynthesis
  • TCA cycle
  • electron transport chain (ETC)
  • mitochondrial potential
  • mitochondrial reactive oxygen species (mtROS)
  • mitochondrial DNA (mtDNA)
  • mtDNA mutations
  • mtDNA repair
  • mtDNA epigenetics
  • mitochondrial fusion
  • mitochondrial fission
  • mitophagy
  • mitochondrial transfer
  • homoplasmy
  • heteroplasmy
  • apoptosis
  • tumorigenesis
  • chemoresistance
  • radioresistance
  • cancer stem cells
  • metastatic progenitor cells

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Published Papers (6 papers)

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15 pages, 2574 KiB  
Article
Aspirin Induces Mitochondrial Ca2+ Remodeling in Tumor Cells via ROS‒Depolarization‒Voltage-Gated Ca2+ Entry
by Itsuho Fujikawa, Takashi Ando, Manami Suzuki-Karasaki, Miki Suzuki-Karasaki, Toyoko Ochiai and Yoshihiro Suzuki-Karasaki
Int. J. Mol. Sci. 2020, 21(13), 4771; https://doi.org/10.3390/ijms21134771 - 5 Jul 2020
Cited by 13 | Viewed by 3767
Abstract
Aspirin (acetylsalicylic acid) and its metabolite salicylate, have an anti-melanoma effect by evoking mitochondrial dysfunction through poorly understood mechanisms. Depolarization of the plasma membrane potential leads to voltage-gated Ca2+ entry (VGCE) and caspase-3 activation. In the present study, we investigated the role [...] Read more.
Aspirin (acetylsalicylic acid) and its metabolite salicylate, have an anti-melanoma effect by evoking mitochondrial dysfunction through poorly understood mechanisms. Depolarization of the plasma membrane potential leads to voltage-gated Ca2+ entry (VGCE) and caspase-3 activation. In the present study, we investigated the role of depolarization and VGCE in aspirin’s anti-melanoma effect. Aspirin and to a lesser extent, salicylate (≥2.5 mM) induced a rapid (within seconds) depolarization, while they caused comparable levels of depolarization with a lag of 2~4 h. Reactive oxygen species (ROS) generation also occurred in the two-time points, and antioxidants abolished the early ROS generation and depolarization. At the same concentrations, the two drugs induced apoptotic and necrotic cell death in a caspase-independent manner, and antioxidants and Ca2+ channel blockers prevented cell death. Besides ROS generation, reduced mitochondrial Ca2+ (Ca2+m) and mitochondrial membrane potential preceded cell death. Moreover, the cells expressed the Cav1.2 isoform of l-type Ca2+ channel, and knockdown of Cav1.2 abolished the decrease in Ca2+m. Our findings suggest that aspirin and salicylate induce Ca2+m remodeling, mitochondrial dysfunction, and cell death via ROS-dependent depolarization and VGCE activation. Full article
(This article belongs to the Special Issue Mitochondrial Functions, Alterations and Dynamics in Cancer)
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Review

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22 pages, 2207 KiB  
Review
Melatonin and Pathological Cell Interactions: Mitochondrial Glucose Processing in Cancer Cells
by Russel J Reiter, Ramaswamy Sharma, Sergio Rosales-Corral, Walter Manucha, Luiz Gustavo de Almeida Chuffa and Debora Aparecida Pires de Campos Zuccari
Int. J. Mol. Sci. 2021, 22(22), 12494; https://doi.org/10.3390/ijms222212494 - 19 Nov 2021
Cited by 33 | Viewed by 9344
Abstract
Melatonin is synthesized in the pineal gland at night. Since melatonin is produced in the mitochondria of all other cells in a non-circadian manner, the amount synthesized by the pineal gland is less than 5% of the total. Melatonin produced in mitochondria influences [...] Read more.
Melatonin is synthesized in the pineal gland at night. Since melatonin is produced in the mitochondria of all other cells in a non-circadian manner, the amount synthesized by the pineal gland is less than 5% of the total. Melatonin produced in mitochondria influences glucose metabolism in all cells. Many pathological cells adopt aerobic glycolysis (Warburg effect) in which pyruvate is excluded from the mitochondria and remains in the cytosol where it is metabolized to lactate. The entrance of pyruvate into the mitochondria of healthy cells allows it to be irreversibly decarboxylated by pyruvate dehydrogenase (PDH) to acetyl coenzyme A (acetyl-CoA). The exclusion of pyruvate from the mitochondria in pathological cells prevents the generation of acetyl-CoA from pyruvate. This is relevant to mitochondrial melatonin production, as acetyl-CoA is a required co-substrate/co-factor for melatonin synthesis. When PDH is inhibited during aerobic glycolysis or during intracellular hypoxia, the deficiency of acetyl-CoA likely prevents mitochondrial melatonin synthesis. When cells experiencing aerobic glycolysis or hypoxia with a diminished level of acetyl-CoA are supplemented with melatonin or receive it from another endogenous source (pineal-derived), pathological cells convert to a more normal phenotype and support the transport of pyruvate into the mitochondria, thereby re-establishing a healthier mitochondrial metabolic physiology. Full article
(This article belongs to the Special Issue Mitochondrial Functions, Alterations and Dynamics in Cancer)
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27 pages, 2238 KiB  
Review
The Interplay between Dysregulated Ion Transport and Mitochondrial Architecture as a Dangerous Liaison in Cancer
by Stine F. Pedersen, Mette Flinck and Luis A. Pardo
Int. J. Mol. Sci. 2021, 22(10), 5209; https://doi.org/10.3390/ijms22105209 - 14 May 2021
Cited by 18 | Viewed by 4569
Abstract
Transport of ions and nutrients is a core mitochondrial function, without which there would be no mitochondrial metabolism and ATP production. Both ion homeostasis and mitochondrial phenotype undergo pervasive changes during cancer development, and both play key roles in driving the malignancy. However, [...] Read more.
Transport of ions and nutrients is a core mitochondrial function, without which there would be no mitochondrial metabolism and ATP production. Both ion homeostasis and mitochondrial phenotype undergo pervasive changes during cancer development, and both play key roles in driving the malignancy. However, the link between these events has been largely ignored. This review comprehensively summarizes and critically discusses the role of the reciprocal relationship between ion transport and mitochondria in crucial cellular functions, including metabolism, signaling, and cell fate decisions. We focus on Ca2+, H+, and K+, which play essential and highly interconnected roles in mitochondrial function and are profoundly dysregulated in cancer. We describe the transport and roles of these ions in normal mitochondria, summarize the changes occurring during cancer development, and discuss how they might impact tumorigenesis. Full article
(This article belongs to the Special Issue Mitochondrial Functions, Alterations and Dynamics in Cancer)
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14 pages, 895 KiB  
Review
Hexokinase 2 in Cancer: A Prima Donna Playing Multiple Characters
by Francesco Ciscato, Lavinia Ferrone, Ionica Masgras, Claudio Laquatra and Andrea Rasola
Int. J. Mol. Sci. 2021, 22(9), 4716; https://doi.org/10.3390/ijms22094716 - 29 Apr 2021
Cited by 142 | Viewed by 13573
Abstract
Hexokinases are a family of ubiquitous exose-phosphorylating enzymes that prime glucose for intracellular utilization. Hexokinase 2 (HK2) is the most active isozyme of the family, mainly expressed in insulin-sensitive tissues. HK2 induction in most neoplastic cells contributes to their metabolic rewiring towards aerobic [...] Read more.
Hexokinases are a family of ubiquitous exose-phosphorylating enzymes that prime glucose for intracellular utilization. Hexokinase 2 (HK2) is the most active isozyme of the family, mainly expressed in insulin-sensitive tissues. HK2 induction in most neoplastic cells contributes to their metabolic rewiring towards aerobic glycolysis, and its genetic ablation inhibits malignant growth in mouse models. HK2 can dock to mitochondria, where it performs additional functions in autophagy regulation and cell death inhibition that are independent of its enzymatic activity. The recent definition of HK2 localization to contact points between mitochondria and endoplasmic reticulum called Mitochondria Associated Membranes (MAMs) has unveiled a novel HK2 role in regulating intracellular Ca2+ fluxes. Here, we propose that HK2 localization in MAMs of tumor cells is key in sustaining neoplastic progression, as it acts as an intersection node between metabolic and survival pathways. Disrupting these functions by targeting HK2 subcellular localization can constitute a promising anti-tumor strategy. Full article
(This article belongs to the Special Issue Mitochondrial Functions, Alterations and Dynamics in Cancer)
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14 pages, 3699 KiB  
Review
Mitochondrial Transfer in Cancer: A Comprehensive Review
by Luca X. Zampieri, Catarina Silva-Almeida, Justin D. Rondeau and Pierre Sonveaux
Int. J. Mol. Sci. 2021, 22(6), 3245; https://doi.org/10.3390/ijms22063245 - 23 Mar 2021
Cited by 100 | Viewed by 11533
Abstract
Depending on their tissue of origin, genetic and epigenetic marks and microenvironmental influences, cancer cells cover a broad range of metabolic activities that fluctuate over time and space. At the core of most metabolic pathways, mitochondria are essential organelles that participate in energy [...] Read more.
Depending on their tissue of origin, genetic and epigenetic marks and microenvironmental influences, cancer cells cover a broad range of metabolic activities that fluctuate over time and space. At the core of most metabolic pathways, mitochondria are essential organelles that participate in energy and biomass production, act as metabolic sensors, control cancer cell death, and initiate signaling pathways related to cancer cell migration, invasion, metastasis and resistance to treatments. While some mitochondrial modifications provide aggressive advantages to cancer cells, others are detrimental. This comprehensive review summarizes the current knowledge about mitochondrial transfers that can occur between cancer and nonmalignant cells. Among different mechanisms comprising gap junctions and cell-cell fusion, tunneling nanotubes are increasingly recognized as a main intercellular platform for unidirectional and bidirectional mitochondrial exchanges. Understanding their structure and functionality is an important task expected to generate new anticancer approaches aimed at interfering with gains of functions (e.g., cancer cell proliferation, migration, invasion, metastasis and chemoresistance) or damaged mitochondria elimination associated with mitochondrial transfer. Full article
(This article belongs to the Special Issue Mitochondrial Functions, Alterations and Dynamics in Cancer)
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16 pages, 1951 KiB  
Review
Cardiolipin, the Mitochondrial Signature Lipid: Implication in Cancer
by Seyedeh Tayebeh Ahmadpour, Karine Mahéo, Stéphane Servais, Lucie Brisson and Jean-François Dumas
Int. J. Mol. Sci. 2020, 21(21), 8031; https://doi.org/10.3390/ijms21218031 - 28 Oct 2020
Cited by 55 | Viewed by 7826
Abstract
Cardiolipins (CLs) are specific phospholipids of the mitochondria composing about 20% of the inner mitochondria membrane (IMM) phospholipid mass. Dysregulation of CL metabolism has been observed in several types of cancer. In most cases, the evidence for a role for CL in cancer [...] Read more.
Cardiolipins (CLs) are specific phospholipids of the mitochondria composing about 20% of the inner mitochondria membrane (IMM) phospholipid mass. Dysregulation of CL metabolism has been observed in several types of cancer. In most cases, the evidence for a role for CL in cancer is merely correlative, suggestive, ambiguous, and cancer-type dependent. In addition, CLs could play a pivotal role in several mitochondrial functions/parameters such as bioenergetics, dynamics, mitophagy, and apoptosis, which are involved in key steps of cancer aggressiveness (i.e., migration/invasion and resistance to treatment). Therefore, this review focuses on studies suggesting that changes in CL content and/or composition, as well as CL metabolism enzyme levels, may be linked with the progression and the aggressiveness of some types of cancer. Finally, we also introduce the main mitochondrial function in which CL could play a pivotal role with a special focus on its implication in cancer development and therapy. Full article
(This article belongs to the Special Issue Mitochondrial Functions, Alterations and Dynamics in Cancer)
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