Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.0
4.5
Journals
Cancers
Special Issues
Mitochondrial Functions in Cancer
share announcement

Mitochondrial Functions in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Epidemiology and Prevention".

Deadline for manuscript submissions: closed (1 October 2024) | Viewed by 24544

Special Issue Editors

Prof. Dr. Pierre Sonveaux

E-Mail Website
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
Prof. Dr. Rodrigue Rossignol

E-Mail Website
Guest Editor
INSERM U1211, Laboratory of Rare Diseases, Metabolism and Genetics (MRGM), Ecole des Sages Femmes, Bordeaux University, 33076 Bordeaux, France
Interests: bioenergetics; targeting mitochondria in cancer; mitochondrial modulation and medicine; REDOX signaling; metabolic reprogramming
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Mitochondria are bioenergetic organelles that are believed to originate from a symbiotic relationship established between archebacteria and the ancestors of eukaryotic cells. They comprise an outer and an inner membrane that delineate an intermembrane space, and an inner matrix hosting a short, circular DNA and several enzymes orchestrating, e.g., the tricarboxylic acid (TCA) cycle. Oxygen-dependent respiration for ATP production occurs at the electron transfer chain (ETC) localized at the inner mitochondrial membrane. Besides bioenergetics, mitochondria also control several other key cellular functions, comprising apoptosis, calcium homeostasis, iron metabolism and redox signaling. Their subcellular location changes depending on cell activities. Upon damage, their renewal involves mitochondrial selective autophagy (mitophagy) and mitochondrial biogenesis.

In tumors, cancer cells (and host cells) strive to simultaneously ensure optimal energy production and biosynthesis with local resources that are often limited. The balance between these activities depends on mitochondrial functions that can oscillate between ATP production and biosynthesis. Mitochondria also participate in cancer cell immortalization and may act as metabolic sensors of the tumor microenvironment. Upon treatment, they can be damaged and repaired, thus participating in resistance to therapy. This Topic issue in Cancers aims to address these functions, with a key interest for the relationship between mitochondria and specific phenotypic changes occurring during tumor growth and treatment.

Prof. Dr. Pierre Sonveaux
Prof. Dr. Rodrigue Rossignol
Guest Editors

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 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

  • cancer
  • mitochondria
  • mitochondrial DNA
  • TCA cycle
  • electron transport chain
  • apoptosis
  • calcium homeostasis
  • mitophagy
  • mitochondrial biogenesis
  • fission
  • fusion

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

20 pages, 5695 KiB  
Article
Contribution of Mitochondrial Activity to Doxorubicin-Resistance in Osteosarcoma Cells
by Isabella Giacomini, Margherita Cortini, Mattia Tinazzi, Nicola Baldini, Veronica Cocetta, Eugenio Ragazzi, Sofia Avnet and Monica Montopoli
Cancers 2023, 15(5), 1370; https://doi.org/10.3390/cancers15051370 - 21 Feb 2023
Cited by 4 | Viewed by 2537
Abstract
Osteosarcoma is considered the most common bone tumor affecting children and young adults. The standard of care is chemotherapy; however, the onset of drug resistance still jeopardizes osteosarcoma patients, thus making it necessary to conduct a thorough investigation of the possible mechanisms behind [...] Read more.
Osteosarcoma is considered the most common bone tumor affecting children and young adults. The standard of care is chemotherapy; however, the onset of drug resistance still jeopardizes osteosarcoma patients, thus making it necessary to conduct a thorough investigation of the possible mechanisms behind this phenomenon. In the last decades, metabolic rewiring of cancer cells has been proposed as a cause of chemotherapy resistance. Our aim was to compare the mitochondrial phenotype of sensitive osteosarcoma cells (HOS and MG-63) versus their clones when continuously exposed to doxorubicin (resistant cells) and identify alterations exploitable for pharmacological approaches to overcome chemotherapy resistance. Compared with sensitive cells, doxorubicin-resistant clones showed sustained viability with less oxygen-dependent metabolisms, and significantly reduced mitochondrial membrane potential, mitochondrial mass, and ROS production. In addition, we found reduced expression of TFAM gene generally associated with mitochondrial biogenesis. Finally, combined treatment of resistant osteosarcoma cells with doxorubicin and quercetin, a known inducer of mitochondrial biogenesis, re-sensitizes the doxorubicin effect in resistant cells. Despite further investigations being needed, these results pave the way for the use of mitochondrial inducers as a promising strategy to re-sensitize doxorubicin cytotoxicity in patients who do not respond to therapy or reduce doxorubicin side effects. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Cancer)
►▼ Show Figures

Graphical abstract

20 pages, 32586 KiB  
Article
Inhibition of Mitochondrial Redox Signaling with MitoQ Prevents Metastasis of Human Pancreatic Cancer in Mice
by Tania Capeloa, Justine A. Van de Velde, Donatienne d’Hose, Sara G. Lipari, Françoise Derouane, Loïc Hamelin, Marie Bedin, Thibaut Vazeille, François P. Duhoux, Michael P. Murphy, Paolo E. Porporato, Bernard Gallez and Pierre Sonveaux
Cancers 2022, 14(19), 4918; https://doi.org/10.3390/cancers14194918 - 7 Oct 2022
Cited by 16 | Viewed by 3086
Abstract
At diagnosis, about 35% of pancreatic cancers are at the locally invasive yet premetastatic stage. Surgical resection is not a treatment option, leaving patients with a largely incurable disease that often evolves to the polymetastatic stage despite chemotherapeutic interventions. In this preclinical study, [...] Read more.
At diagnosis, about 35% of pancreatic cancers are at the locally invasive yet premetastatic stage. Surgical resection is not a treatment option, leaving patients with a largely incurable disease that often evolves to the polymetastatic stage despite chemotherapeutic interventions. In this preclinical study, we hypothesized that pancreatic cancer metastasis can be prevented by inhibiting mitochondrial redox signaling with MitoQ, a mitochondria-targeted antioxidant. Using four different cancer cell lines, we report that, at clinically relevant concentrations (100–500 nM), MitoQ selectively repressed mesenchymal pancreatic cancer cell respiration, which involved the inhibition of the expression of PGC-1α, NRF1 and a reduced expression of electron-transfer-chain complexes I to III. MitoQ consequently decreased the mitochondrial membrane potential and mitochondrial superoxide production by these cells. Phenotypically, MitoQ further inhibited pancreatic cancer cell migration, invasion, clonogenicity and the expression of stem cell markers. It reduced by ~50% the metastatic homing of human MIA PaCa-2 cells in the lungs of mice. We further show that combination treatments with chemotherapy are conceivable. Collectively, this study indicates that the inhibition of mitochondrial redox signaling is a possible therapeutic option to inhibit the metastatic progression of pancreatic cancer. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Cancer)
►▼ Show Figures

Figure 1

Review

Jump to: Research

29 pages, 828 KiB  
Review
Unraveling the Peculiar Features of Mitochondrial Metabolism and Dynamics in Prostate Cancer
by Fabrizio Fontana, Martina Anselmi and Patrizia Limonta
Cancers 2023, 15(4), 1192; https://doi.org/10.3390/cancers15041192 - 13 Feb 2023
Cited by 5 | Viewed by 2693
Abstract
Prostate cancer (PCa) is the second leading cause of cancer deaths among men in Western countries. Mitochondria, the “powerhouse” of cells, undergo distinctive metabolic and structural dynamics in different types of cancer. PCa cells experience peculiar metabolic changes during their progression from normal [...] Read more.
Prostate cancer (PCa) is the second leading cause of cancer deaths among men in Western countries. Mitochondria, the “powerhouse” of cells, undergo distinctive metabolic and structural dynamics in different types of cancer. PCa cells experience peculiar metabolic changes during their progression from normal epithelial cells to early-stage and, progressively, to late-stage cancer cells. Specifically, healthy cells display a truncated tricarboxylic acid (TCA) cycle and inefficient oxidative phosphorylation (OXPHOS) due to the high accumulation of zinc that impairs the activity of m-aconitase, the enzyme of the TCA cycle responsible for the oxidation of citrate. During the early phase of cancer development, intracellular zinc levels decrease leading to the reactivation of m-aconitase, TCA cycle and OXPHOS. PCa cells change their metabolic features again when progressing to the late stage of cancer. In particular, the Warburg effect was consistently shown to be the main metabolic feature of late-stage PCa cells. However, accumulating evidence sustains that both the TCA cycle and the OXPHOS pathway are still present and active in these cells. The androgen receptor axis as well as mutations in mitochondrial genes involved in metabolic rewiring were shown to play a key role in PCa cell metabolic reprogramming. Mitochondrial structural dynamics, such as biogenesis, fusion/fission and mitophagy, were also observed in PCa cells. In this review, we focus on the mitochondrial metabolic and structural dynamics occurring in PCa during tumor development and progression; their role as effective molecular targets for novel therapeutic strategies in PCa patients is also discussed. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Cancer)
►▼ Show Figures

Figure 1

28 pages, 931 KiB  
Review
Metabolic Health, Mitochondrial Fitness, Physical Activity, and Cancer
by Vicente Javier Clemente-Suárez, Alexandra Martín-Rodríguez, Laura Redondo-Flórez, Pablo Ruisoto, Eduardo Navarro-Jiménez, Domingo Jesús Ramos-Campo and José Francisco Tornero-Aguilera
Cancers 2023, 15(3), 814; https://doi.org/10.3390/cancers15030814 - 28 Jan 2023
Cited by 16 | Viewed by 5046
Abstract
Cancer continues to be a significant global health issue. Traditional genetic-based approaches to understanding and treating cancer have had limited success. Researchers are increasingly exploring the impact of the environment, specifically inflammation and metabolism, on cancer development. Examining the role of mitochondria in [...] Read more.
Cancer continues to be a significant global health issue. Traditional genetic-based approaches to understanding and treating cancer have had limited success. Researchers are increasingly exploring the impact of the environment, specifically inflammation and metabolism, on cancer development. Examining the role of mitochondria in this context is crucial for understanding the connections between metabolic health, physical activity, and cancer. This study aimed to review the literature on this topic through a comprehensive narrative review of various databases including MedLine (PubMed), Cochrane (Wiley), Embase, PsychINFO, and CinAhl. The review highlighted the importance of mitochondrial function in overall health and in regulating key events in cancer development, such as apoptosis. The concept of “mitochondrial fitness” emphasizes the crucial role of mitochondria in cell metabolism, particularly their oxidative functions, and how proper function can prevent replication errors and regulate apoptosis. Engaging in high-energy-demanding movement, such as exercise, is a powerful intervention for improving mitochondrial function and increasing resistance to environmental stressors. These findings support the significance of considering the role of the environment, specifically inflammation and metabolism, in cancer development and treatment. Further research is required to fully understand the mechanisms by which physical activity improves mitochondrial function and potentially reduces the risk of cancer. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Cancer)
►▼ Show Figures

Figure 1

18 pages, 1231 KiB  
Review
Lipid Metabolism Heterogeneity and Crosstalk with Mitochondria Functions Drive Breast Cancer Progression and Drug Resistance
by Aurelien Azam and Nor Eddine Sounni
Cancers 2022, 14(24), 6267; https://doi.org/10.3390/cancers14246267 - 19 Dec 2022
Cited by 7 | Viewed by 3162
Abstract
Breast cancer (BC) is a heterogeneous disease that can be triggered by genetic alterations in mammary epithelial cells, leading to diverse disease outcomes in individual patients. The metabolic heterogeneity of BC enhances its ability to adapt to changes in the tumor microenvironment and [...] Read more.
Breast cancer (BC) is a heterogeneous disease that can be triggered by genetic alterations in mammary epithelial cells, leading to diverse disease outcomes in individual patients. The metabolic heterogeneity of BC enhances its ability to adapt to changes in the tumor microenvironment and metabolic stress, but unfavorably affects the patient’s therapy response, prognosis and clinical effect. Extrinsic factors from the tumor microenvironment and the intrinsic parameters of cancer cells influence their mitochondrial functions, which consequently alter their lipid metabolism and their ability to proliferate, migrate and survive in a harsh environment. The balanced interplay between mitochondria and fatty acid synthesis or fatty acid oxidation has been attributed to a combination of environmental factors and to the genetic makeup, oncogenic signaling and activities of different transcription factors. Hence, understanding the mechanisms underlying lipid metabolic heterogeneity and alterations in BC is gaining interest as a major target for drug resistance. Here we review the major recent reports on lipid metabolism heterogeneity and bring to light knowledge on the functional contribution of diverse lipid metabolic pathways to breast tumorigenesis and therapy resistance. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Cancer)
►▼ Show Figures

Figure 1

21 pages, 3153 KiB  
Review
Revisiting the Warburg Effect with Focus on Lactate
by Eva Kocianova, Viktoria Piatrikova and Tereza Golias
Cancers 2022, 14(24), 6028; https://doi.org/10.3390/cancers14246028 - 7 Dec 2022
Cited by 27 | Viewed by 6958
Abstract
Rewired metabolism is acknowledged as one of the drivers of tumor growth. As a result, aerobic glycolysis, or the Warburg effect, is a feature of many cancers. Increased glucose uptake and glycolysis provide intermediates for anabolic reactions necessary for cancer cell proliferation while [...] Read more.
Rewired metabolism is acknowledged as one of the drivers of tumor growth. As a result, aerobic glycolysis, or the Warburg effect, is a feature of many cancers. Increased glucose uptake and glycolysis provide intermediates for anabolic reactions necessary for cancer cell proliferation while contributing sufficient energy. However, the accompanying increased lactate production, seemingly wasting glucose carbon, was originally explained only by the need to regenerate NAD+ for successive rounds of glycolysis by the lactate dehydrogenase (LDH) reaction in the cytosol. After the discovery of a mitochondrial LDH isoform, lactate oxidation entered the picture, and lactate was recognized as an important oxidative fuel. It has also been revealed that lactate serves a variety of signaling functions and helps cells adapt to the new environment. Here, we discuss recent findings on lactate metabolism and signaling in cancer while attempting to explain why the Warburg effect is adopted by cancer cells. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Cancer)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop