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Cancers
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Mitochondria and Cancer
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Mitochondria and Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (15 November 2019) | Viewed by 38331

Special Issue Editor

Prof. Dr. Alexandr V. Bazhin

E-Mail Website
Guest Editor
Department of General, Visceral, and Transplant Surgery, Ludwig-Maximilians-University Munich, Marchioninistraße 15, 81377 Munich, Germany
Interests: cancer immunology and biochemistry; reactive oxygen species; transplant immunology; cancer immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are indispensable for energy metabolism and are essential for the regulation of many cellular processes in healthy as well as transformed cells. Mitochondria in malignant cells differ structurally and functionally from those in normal cells, which makes them a promising target for anticancer therapy. Mitochondria in cancer cells are characterized by reactive oxygen species (ROS) overproduction, which promotes cancer development by inducing genomic instability, modifying gene expression, and participating in signaling pathways. Also, the pleiotropic roles of mitochondrial ROS in the regulation of anticancer immunity are now coming to light. The involvement of mitochondria in cancer cell metabolic reprogramming as well as in the anticancer immune response has been utilized for designing novel mitochondria-targeted anticancer agents. However, we are still far from attaining a deep understanding of the role played by mitochondria in cancer development. The main aim of this Special Issue is to collect novel findings from scientists involved in basic research as well as in translational studies in field of mitochondria and cancer.

Prof. Dr. Alexandr V. Bazhin
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondria
  • reactive oxygen species
  • antioxidants
  • cancer metabolisms
  • tumor microenvironment
  • metabolic checkpoints

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

2 pages, 152 KiB  
Editorial
Mitochondria and Cancer
by Alexandr V. Bazhin
Cancers 2020, 12(9), 2641; https://doi.org/10.3390/cancers12092641 - 16 Sep 2020
Cited by 7 | Viewed by 1620
Abstract
Mitochondria are indispensable for energy metabolism and are essential for the regulation of many cellular processes in healthy as well as in transformed cells [...] Full article
(This article belongs to the Special Issue Mitochondria and Cancer)

Research

Jump to: Editorial, Review

14 pages, 2359 KiB  
Article
Oncogenic K-ras Induces Mitochondrial OPA3 Expression to Promote Energy Metabolism in Pancreatic Cancer Cells
by Ning Meng, Christophe Glorieux, Yanyu Zhang, Liyun Liang, Peiting Zeng, Wenhua Lu and Peng Huang
Cancers 2020, 12(1), 65; https://doi.org/10.3390/cancers12010065 - 25 Dec 2019
Cited by 17 | Viewed by 3509
Abstract
K-ras (Kirsten ras GTPase) mutations are oncogenic events frequently observed in many cancer types especially in pancreatic cancer. Although mitochondrial dysfunction has been associated with K-ras mutation, the molecular mechanisms by which K-ras impacts mitochondria and maintains metabolic homeostasis are not fully understood. [...] Read more.
K-ras (Kirsten ras GTPase) mutations are oncogenic events frequently observed in many cancer types especially in pancreatic cancer. Although mitochondrial dysfunction has been associated with K-ras mutation, the molecular mechanisms by which K-ras impacts mitochondria and maintains metabolic homeostasis are not fully understood. In this study, we used two K-ras inducible cell systems, human pancreatic epithelial/ K-rasG12D (HPNE/K-rasG12D) and human embryonic kidney cells with tetracycline repressorT-Rex/K-rasG12V, to evaluate the role of oncogenic K-ras in regulating mitochondrial function. Among a panel of genes known to affect mitochondria, only the expression of OPA3 (optic atrophy protein 3) was consistently up-regulated by K-ras activation in both cell lines. Importantly, high expression of OPA3 was also observed in clinical pancreatic cancer tissues. Genetic knockdown of OPA3 caused a significant decrease of energy metabolism, manifested by a suppression of oxygen consumption rate (OCR) and a decrease in cellular ATP content, leading to inhibition of cell proliferation capacity and reduced expression of epithelial–mesenchymal transition (EMT) markers. Our study suggests that OPA3 may promote cellular energy metabolism and its up-regulation in K-ras-driven cancer is likely a mechanism to offset the negative impact of K-ras on mitochondria to maintain energy homeostasis. As such, OPA3 could be a potential target to kill cancer cells with K-ras mutations. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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15 pages, 5456 KiB  
Article
3D Quantitative and Ultrastructural Analysis of Mitochondria in a Model of Doxorubicin Sensitive and Resistant Human Colon Carcinoma Cells
by Claudia Moscheni, Emil Malucelli, Sara Castiglioni, Alessandra Procopio, Clara De Palma, Andrea Sorrentino, Patrizia Sartori, Laura Locatelli, Eva Pereiro, Jeanette A. Maier and Stefano Iotti
Cancers 2019, 11(9), 1254; https://doi.org/10.3390/cancers11091254 - 27 Aug 2019
Cited by 14 | Viewed by 4610
Abstract
Drug resistance remains a major obstacle in cancer treatment. Because mitochondria mediate metabolic reprogramming in cancer drug resistance, we focused on these organelles in doxorubicin sensitive and resistant colon carcinoma cells. We employed soft X-ray cryo nano-tomography to map three-dimensionally these cells at [...] Read more.
Drug resistance remains a major obstacle in cancer treatment. Because mitochondria mediate metabolic reprogramming in cancer drug resistance, we focused on these organelles in doxorubicin sensitive and resistant colon carcinoma cells. We employed soft X-ray cryo nano-tomography to map three-dimensionally these cells at nanometer-resolution and investigate the correlation between mitochondrial morphology and drug resistance phenotype. We have identified significant structural differences in the morphology of mitochondria in the two strains of cancer cells, as well as lower amounts of Reactive oxygen species (ROS) in resistant than in sensitive cells. We speculate that these features could elicit an impaired mitochondrial communication in resistant cells, thus preventing the formation of the interconnected mitochondrial network as clearly detected in the sensitive cells. In fact, the qualitative and quantitative three-dimensional assessment of the mitochondrial morphology highlights a different structural organization in resistant cells, which reflects a metabolic cellular adaptation functional to survive to the offense exerted by the antineoplastic treatment. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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Review

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20 pages, 3809 KiB  
Review
Recent Progress in Mitochondria-Targeted Drug and Drug-Free Agents for Cancer Therapy
by M.T. Jeena, Sangpil Kim, Seongeon Jin and Ja-Hyoung Ryu
Cancers 2020, 12(1), 4; https://doi.org/10.3390/cancers12010004 - 18 Dec 2019
Cited by 91 | Viewed by 10232
Abstract
The mitochondrion is a dynamic eukaryotic organelle that controls lethal and vital functions of the cell. Being a critical center of metabolic activities and involved in many diseases, mitochondria have been attracting attention as a potential target for therapeutics, especially for cancer treatment. [...] Read more.
The mitochondrion is a dynamic eukaryotic organelle that controls lethal and vital functions of the cell. Being a critical center of metabolic activities and involved in many diseases, mitochondria have been attracting attention as a potential target for therapeutics, especially for cancer treatment. Structural and functional differences between healthy and cancerous mitochondria, such as membrane potential, respiratory rate, energy production pathway, and gene mutations, could be employed for the design of selective targeting systems for cancer mitochondria. A number of mitochondria-targeting compounds, including mitochondria-directed conventional drugs, mitochondrial proteins/metabolism-inhibiting agents, and mitochondria-targeted photosensitizers, have been discussed. Recently, certain drug-free approaches have been introduced as an alternative to induce selective cancer mitochondria dysfunction, such as intramitochondrial aggregation, self-assembly, and biomineralization. In this review, we discuss the recent progress in mitochondria-targeted cancer therapy from the conventional approach of drug/cytotoxic agent conjugates to advanced drug-free approaches. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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21 pages, 2146 KiB  
Review
Sestrins as a Therapeutic Bridge between ROS and Autophagy in Cancer
by Miguel Sánchez-Álvarez, Raffaele Strippoli, Massimo Donadelli, Alexandr V. Bazhin and Marco Cordani
Cancers 2019, 11(10), 1415; https://doi.org/10.3390/cancers11101415 - 22 Sep 2019
Cited by 39 | Viewed by 6661
Abstract
The regulation of Reactive Oxygen Species (ROS) levels and the contribution therein from networks regulating cell metabolism, such as autophagy and the mTOR-dependent nutrient-sensing pathway, constitute major targets for selective therapeutic intervention against several types of tumors, due to their extensive rewiring in [...] Read more.
The regulation of Reactive Oxygen Species (ROS) levels and the contribution therein from networks regulating cell metabolism, such as autophagy and the mTOR-dependent nutrient-sensing pathway, constitute major targets for selective therapeutic intervention against several types of tumors, due to their extensive rewiring in cancer cells as compared to healthy cells. Here, we discuss the sestrin family of proteins—homeostatic transducers of oxidative stress, and drivers of antioxidant and metabolic adaptation—as emerging targets for pharmacological intervention. These adaptive regulators lie at the intersection of those two priority nodes of interest in antitumor intervention—ROS control and the regulation of cell metabolism and autophagy—therefore, they hold the potential not only for the development of completely novel compounds, but also for leveraging on synergistic strategies with current options for tumor therapy and classification/stadiation to achieve personalized medicine. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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28 pages, 499 KiB  
Review
The Importance of Gender-Related Anticancer Research on Mitochondrial Regulator Sodium Dichloroacetate in Preclinical Studies In Vivo
by Donatas Stakišaitis, Milda Juknevičienė, Eligija Damanskienė, Angelija Valančiūtė, Ingrida Balnytė and Marta Maria Alonso
Cancers 2019, 11(8), 1210; https://doi.org/10.3390/cancers11081210 - 20 Aug 2019
Cited by 11 | Viewed by 4270
Abstract
Sodium dichloroacetate (DCA) is an investigational medicinal product which has a potential anticancer preparation as a metabolic regulator in cancer cells’ mitochondria. Inhibition of pyruvate dehydrogenase kinases by DCA keeps the pyruvate dehydrogenase complex in the active form, resulting in decreased lactic acid [...] Read more.
Sodium dichloroacetate (DCA) is an investigational medicinal product which has a potential anticancer preparation as a metabolic regulator in cancer cells’ mitochondria. Inhibition of pyruvate dehydrogenase kinases by DCA keeps the pyruvate dehydrogenase complex in the active form, resulting in decreased lactic acid in the tumor microenvironment. This literature review displays the preclinical research data on DCA’s effects on the cell pyruvate dehydrogenase deficiency, pyruvate mitochondrial oxidative phosphorylation, reactive oxygen species generation, and the Na+–K+–2Cl− cotransporter expression regulation in relation to gender. It presents DCA pharmacokinetics and the hepatocarcinogenic effect, and the safety data covers the DCA monotherapy efficacy for various human cancer xenografts in vivo in male and female animals. Preclinical cancer researchers report the synergistic effects of DCA combined with different drugs on cancer by reversing resistance to chemotherapy and promoting cell apoptosis. Researchers note that female and male animals differ in the mechanisms of cancerogenesis but often ignore studying DCA’s effects in relation to gender. Preclinical gender-related differences in DCA pharmacology, pharmacological mechanisms, and the elucidation of treatment efficacy in gonad hormone dependency could be relevant for individualized therapy approaches so that gender-related differences in treatment response and safety can be proposed. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
20 pages, 669 KiB  
Review
Exploiting Mitochondrial Vulnerabilities to Trigger Apoptosis Selectively in Cancer Cells
by Christopher Nguyen and Siyaram Pandey
Cancers 2019, 11(7), 916; https://doi.org/10.3390/cancers11070916 - 29 Jun 2019
Cited by 66 | Viewed by 6775
Abstract
The transformation of normal cells to the cancerous stage involves multiple genetic changes or mutations leading to hyperproliferation, resistance to apoptosis, and evasion of the host immune system. However, to accomplish hyperproliferation, cancer cells undergo profound metabolic reprogramming including oxidative glycolysis and acidification [...] Read more.
The transformation of normal cells to the cancerous stage involves multiple genetic changes or mutations leading to hyperproliferation, resistance to apoptosis, and evasion of the host immune system. However, to accomplish hyperproliferation, cancer cells undergo profound metabolic reprogramming including oxidative glycolysis and acidification of the cytoplasm, leading to hyperpolarization of the mitochondrial membrane. The majority of drug development research in the past has focused on targeting DNA replication, repair, and tubulin polymerization to induce apoptosis in cancer cells. Unfortunately, these are not cancer-selective targets. Recently, researchers have started focusing on metabolic, mitochondrial, and oxidative stress vulnerabilities of cancer cells that can be exploited as selective targets for inducing cancer cell death. Indeed, the hyperpolarization of mitochondrial membranes in cancer cells can lead to selective importing of mitocans that can induce apoptotic effects. Herein, we will discuss recent mitochondrial-selective anticancer compounds (mitocans) that have shown selective toxicity against cancer cells. Increased oxidative stress has also been shown to be very effective in selectively inducing cell death in cancer cells. This oxidative stress could lead to mitochondrial dysfunction, which in turn will produce more reactive oxygen species (ROS). This creates a vicious cycle of mitochondrial dysfunction and ROS production, irreversibly leading to cell suicide. We will also explore the possibility of combining these compounds to sensitize cancer cells to the conventional anticancer agents. Mitocans in combination with selective oxidative-stress producing agents could be very effective anticancer treatments with minimal effect on healthy cells. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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