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Mitochondria and Cancer
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Mitochondria and Cancer

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

Deadline for manuscript submissions: closed (25 January 2023) | Viewed by 11868

Special Issue Editor

Dr. Josephine S. Modica-Napolitano

E-Mail Website
Guest Editor
Department of Biology, Merrimack College, North Andover, MA 01845, USA
Interests: mitochondria; bioenergetic function; Warburg effect; mitochondria-targeted cancer chemotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The connection between mitochondria and cancer dates back to the 1930s when Otto Warburg first reported his observations of increased rates of aerobic glycolysis in a variety of tumors and hypothesized that this phenomenon might be due to an impaired respiratory capacity in certain cancer cells. Now, nearly a century later, altered energy metabolism is considered an emerging hallmark of cancer, and a large number of other notable differences in the structure and function of mitochondria between normal and cancer cells have been discovered at the genetic, molecular, and biochemical levels. The purpose of this Special Issue is to provide an overview of the known differences in mitochondria structure and function between normal and cancer cells, and to highlight recent advances in our understanding of the role that mitochondria might play in the development, detection, and treatment of cancer. The submission of either primary research or review articles is encouraged.

Dr. Josephine S. Modica-Napolitano
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • cancer
  • Warburg effect
  • mitochondrial dysfunction in cancer
  • mtDNA mutations
  • mitochondrial bioenergetics
  • tumor metabolism
  • metabolic plasticity
  • cancer detection
  • mitochondria-targeted cancer treatment

Published Papers (4 papers)

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Research

Jump to: Review

17 pages, 2451 KiB  
Article
ONC201-Induced Mitochondrial Dysfunction, Senescence-like Phenotype, and Sensitization of Cultured BT474 Human Breast Cancer Cells to TRAIL
by Artem Mishukov, Irina Odinokova, Ekaterina Mndlyan, Margarita Kobyakova, Serazhutdin Abdullaev, Vitaly Zhalimov, Xenia Glukhova, Vasiliy Galat, Yekaterina Galat, Anatoly Senotov, Roman Fadeev, Artem Artykov, Marine E. Gasparian, Marina Solovieva, Igor Beletsky and Ekhson Holmuhamedov
Int. J. Mol. Sci. 2022, 23(24), 15551; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415551 - 08 Dec 2022
Cited by 5 | Viewed by 1773
Abstract
ONC201, the anticancer drug, targets and activates mitochondrial ATP-dependent caseinolytic peptidase P (ClpP), a serine protease located in the mitochondrial matrix. Given the promise of ONC201 in cancer treatment, we evaluated its effects on the breast ductal carcinoma cell line (BT474). We showed [...] Read more.
ONC201, the anticancer drug, targets and activates mitochondrial ATP-dependent caseinolytic peptidase P (ClpP), a serine protease located in the mitochondrial matrix. Given the promise of ONC201 in cancer treatment, we evaluated its effects on the breast ductal carcinoma cell line (BT474). We showed that the transient single-dose treatment of BT474 cells by 10 µM ONC201 for a period of less than 48 h induced a reversible growth arrest and a transient activation of an integrated stress response indicated by an increased expression of CHOP, ATF4, and GDF-15, and a reduced number of mtDNA nucleoids. A prolonged exposure to the drug (>48 h), however, initiated an irreversible loss of mtDNA, persistent activation of integrated stress response proteins, as well as cell cycle arrest, inhibition of proliferation, and suppression of the intrinsic apoptosis pathway. Since Natural Killer (NK) cells are quickly gaining momentum in cellular anti-cancer therapies, we evaluated the effect of ONC201 on the activity of the peripheral blood derived NK cells. We showed that following the ONC 201 exposure BT474 cells demonstrated enhanced sensitivity toward human NK cells that mediated killing. Together our data revealed that the effects of a single dose of ONC201 are dependent on the duration of exposure, specifically, while short-term exposure led to reversible changes; long-term exposure resulted in irreversible transformation of cells associated with the senescent phenotype. Our data further demonstrated that when used in combination with NK cells, ONC201 created a synergistic anti-cancer effect, thus suggesting its possible benefit in NK-cell based cellular immunotherapies for cancer treatment. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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26 pages, 4265 KiB  
Article
Searching for a Paradigm Shift in Auger-Electron Cancer Therapy with Tumor-Specific Radiopeptides Targeting the Mitochondria and/or the Cell Nucleus
by Célia Fernandes, Elisa Palma, Francisco Silva, Ana Belchior, Catarina I. G. Pinto, Joana F. Guerreiro, Hugo M. Botelho, Filipa Mendes, Paula Raposinho and António Paulo
Int. J. Mol. Sci. 2022, 23(13), 7238; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137238 - 29 Jun 2022
Cited by 6 | Viewed by 2180
Abstract
Although 99mTc is not an ideal Auger electron (AE) emitter for Targeted Radionuclide Therapy (TRT) due to its relatively low Auger electron yield, it can be considered a readily available “model” radionuclide useful to validate the design of new classes of AE-emitting [...] Read more.
Although 99mTc is not an ideal Auger electron (AE) emitter for Targeted Radionuclide Therapy (TRT) due to its relatively low Auger electron yield, it can be considered a readily available “model” radionuclide useful to validate the design of new classes of AE-emitting radioconjugates. With this in mind, we performed a detailed study of the radiobiological effects and mechanisms of cell death induced by the dual-targeted radioconjugates 99mTc-TPP-BBN and 99mTc-AO-BBN (TPP = triphenylphosphonium; AO = acridine orange; BBN = bombesin derivative) in human prostate cancer PC3 cells. 99mTc-TPP-BBN and 99mTc-AO-BBN caused a remarkably high reduction of the survival of PC3 cells when compared with the single-targeted congener 99mTc-BBN, leading to an augmented formation of γH2AX foci and micronuclei. 99mTc-TPP-BBN also caused a reduction of the mtDNA copy number, although it enhanced the ATP production by PC3 cells. These differences can be attributed to the augmented uptake of 99mTc-TPP-BBN in the mitochondria and enhanced uptake of 99mTc-AO-BBN in the nucleus, allowing the irradiation of these radiosensitive organelles with the short path-length AEs emitted by 99mTc. In particular, the results obtained for 99mTc-TPP-BBN reinforce the relevance of targeting the mitochondria to promote stronger radiobiological effects by AE-emitting radioconjugates. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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Review

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31 pages, 1558 KiB  
Review
Mitochondrial Genetic and Epigenetic Regulations in Cancer: Therapeutic Potential
by Alexandra Wagner, Helena Kosnacova, Miroslav Chovanec and Dana Jurkovicova
Int. J. Mol. Sci. 2022, 23(14), 7897; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23147897 - 18 Jul 2022
Cited by 12 | Viewed by 3991
Abstract
Mitochondria are dynamic organelles managing crucial processes of cellular metabolism and bioenergetics. Enabling rapid cellular adaptation to altered endogenous and exogenous environments, mitochondria play an important role in many pathophysiological states, including cancer. Being under the control of mitochondrial and nuclear DNA (mtDNA [...] Read more.
Mitochondria are dynamic organelles managing crucial processes of cellular metabolism and bioenergetics. Enabling rapid cellular adaptation to altered endogenous and exogenous environments, mitochondria play an important role in many pathophysiological states, including cancer. Being under the control of mitochondrial and nuclear DNA (mtDNA and nDNA), mitochondria adjust their activity and biogenesis to cell demands. In cancer, numerous mutations in mtDNA have been detected, which do not inactivate mitochondrial functions but rather alter energy metabolism to support cancer cell growth. Increasing evidence suggests that mtDNA mutations, mtDNA epigenetics and miRNA regulations dynamically modify signalling pathways in an altered microenvironment, resulting in cancer initiation and progression and aberrant therapy response. In this review, we discuss mitochondria as organelles importantly involved in tumorigenesis and anti-cancer therapy response. Tumour treatment unresponsiveness still represents a serious drawback in current drug therapies. Therefore, studying aspects related to genetic and epigenetic control of mitochondria can open a new field for understanding cancer therapy response. The urgency of finding new therapeutic regimens with better treatment outcomes underlines the targeting of mitochondria as a suitable candidate with new therapeutic potential. Understanding the role of mitochondria and their regulation in cancer development, progression and treatment is essential for the development of new safe and effective mitochondria-based therapeutic regimens. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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16 pages, 952 KiB  
Review
The Role of Altered Mitochondrial Metabolism in Thyroid Cancer Development and Mitochondria-Targeted Thyroid Cancer Treatment
by Siarhei A. Dabravolski, Nikita G. Nikiforov, Alexander D. Zhuravlev, Nikolay A. Orekhov, Liudmila M. Mikhaleva and Alexander N. Orekhov
Int. J. Mol. Sci. 2022, 23(1), 460; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010460 - 31 Dec 2021
Cited by 9 | Viewed by 2861
Abstract
Thyroid cancer (TC) is the most common type of endocrine malignancy. Tumour formation, progression, and metastasis greatly depend on the efficacy of mitochondria—primarily, the regulation of mitochondria-mediated apoptosis, Ca2+ homeostasis, dynamics, energy production, and associated reactive oxygen species generation. Recent studies have [...] Read more.
Thyroid cancer (TC) is the most common type of endocrine malignancy. Tumour formation, progression, and metastasis greatly depend on the efficacy of mitochondria—primarily, the regulation of mitochondria-mediated apoptosis, Ca2+ homeostasis, dynamics, energy production, and associated reactive oxygen species generation. Recent studies have successfully confirmed the mitochondrial aetiology of thyroid carcinogenesis. In this review, we focus on the recent progress in understanding the molecular mechanisms of thyroid cancer relating to altered mitochondrial metabolism. We also discuss the repurposing of known drugs and the induction of mitochondria-mediated apoptosis as a new trend in the development of anti-TC therapy. Full article
(This article belongs to the Special Issue Mitochondria and Cancer)
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