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Mitochondrial Metabolic Alterations in Cancer
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Mitochondrial Metabolic Alterations in 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 (29 November 2023) | Viewed by 3578

Special Issue Editors

Prof. Dr. Vincenza Dolce

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Guest Editor
Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy
Interests: mitochondrial transporters; bioenergetics; mitochondrial diseases; cancers metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Rosita Curcio

E-Mail Website
Guest Editor
Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy
Interests: bioenergetics; mitochondrial carriers; mutagenesis, drosophila melanogaster; mitochondrial diseases; mitochondrial dysfunction; apoptosis; ROS; antioxidant and anti-inflammatory activity; cancer metabolism; anticancer agents
Special Issues, Collections and Topics in MDPI journals
Dr. Graziantonio Lauria

E-Mail Website
Guest Editor
Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy
Interests: ketogenic diet; microRNAs signature; catalase; heavy metals metabolic effects; epigenetics; apoptosis; antioxidant effects
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are essential in ATP generation and cellular bioenergetic metabolism, and in the biosynthesis of macromolecules, ROS production, redox balance and apoptotic signaling, which are involved in carcinogenesis. Mitochondria play a critical role in cancer initiation, as mutations in mtDNA and nuclear-encoded mitochondrial genes alter cell metabolism, affect oxidative respiration and promote oxidative stress and epigenetic processes.

Furthermore, mitochondria are involved in cancer promotion and progression, as later stages of tumor progression are rather associated with mitochondrial metabolic reprogramming by oncogenes, mitochondrial dynamics and oxidative stress. In this view, mitochondria can act as “stress sensors” able to influence cancer cell metabolic adaptations to the microenvironment.

Mechanisms underlying cancer initiation, promotion and progression are multiple, complex and should be further investigated. On this basis, mitochondrial metabolism can represent an interesting potential target for cancer therapy.

This Special Issue will focus on investigating mechanisms by which alterations of mitochondrial metabolism can be implicated in cancer initiation, promotion and progression, in order to understand the molecular basis of cancer. We welcome the submission of original research manuscripts and reviews focusing on the implications of alterations in mitochondrial metabolism and dynamics in cancer, as well as those aimed at targeting mitochondrial metabolism as novel promising therapeutic strategies.

Prof. Dr. Vincenza Dolce
Dr. Rosita Curcio
Dr. Graziantonio Lauria
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 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

  • bioenergetics
  • cancer metabolism
  • ROS
  • OXPHOS
  • mitochondrial dysfunction in cancer
  • mtDNA
  • metabolic reprogramming
  • cancer therapy

Published Papers (3 papers)

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Research

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13 pages, 9894 KiB  
Article
Impaired Mitochondrial Function and Marrow Failure in Patients Carrying a Variant of the SRSF4 Gene
by Maurizio Miano, Nadia Bertola, Alice Grossi, Gianluca Dell’Orso, Stefano Regis, Marta Rusmini, Paolo Uva, Diego Vozzi, Francesca Fioredda, Elena Palmisani, Michela Lupia, Marina Lanciotti, Federica Grilli, Fabio Corsolini, Luca Arcuri, Maria Carla Giarratana, Isabella Ceccherini, Carlo Dufour, Enrico Cappelli and Silvia Ravera
Int. J. Mol. Sci. 2024, 25(4), 2083; https://doi.org/10.3390/ijms25042083 - 08 Feb 2024
Viewed by 700
Abstract
Serine/arginine-rich splicing factors (SRSFs) are a family of proteins involved in RNA metabolism, including pre-mRNA constitutive and alternative splicing. The role of SRSF proteins in regulating mitochondrial activity has already been shown for SRSF6, but SRSF4 altered expression has never been reported as [...] Read more.
Serine/arginine-rich splicing factors (SRSFs) are a family of proteins involved in RNA metabolism, including pre-mRNA constitutive and alternative splicing. The role of SRSF proteins in regulating mitochondrial activity has already been shown for SRSF6, but SRSF4 altered expression has never been reported as a cause of bone marrow failure. An 8-year-old patient admitted to the hematology unit because of leukopenia, lymphopenia, and neutropenia showed a missense variant of unknown significance of the SRSF4 gene (p.R235W) found via whole genome sequencing analysis and inherited from the mother who suffered from mild leuko-neutropenia. Both patients showed lower SRSF4 protein expression and altered mitochondrial function and energetic metabolism in primary lymphocytes and Epstein–Barr-virus (EBV)-immortalized lymphoblasts compared to healthy donor (HD) cells, which appeared associated with low mTOR phosphorylation and an imbalance in the proteins regulating mitochondrial biogenesis (i.e., CLUH) and dynamics (i.e., DRP1 and OPA1). Transfection with the wtSRSF4 gene restored mitochondrial function. In conclusion, this study shows that the described variant of the SRSF4 gene is pathogenetic and causes reduced SRSF4 protein expression, which leads to mitochondrial dysfunction. Since mitochondrial function is crucial for hematopoietic stem cell maintenance and some genetic bone marrow failure syndromes display mitochondrial defects, the SRSF4 mutation could have substantially contributed to the clinical phenotype of our patient. Full article
(This article belongs to the Special Issue Mitochondrial Metabolic Alterations in Cancer)
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19 pages, 3655 KiB  
Article
Using Human ‘Personalized’ Cybrids to Identify Drugs/Agents That Can Regulate Chronic Lymphoblastic Leukemia Mitochondrial Dysfunction
by Lata Singh, Shari Atilano, Marilyn Chwa, Mithalesh K. Singh, Mustafa Ozgul, Anthony Nesburn and M. Cristina Kenney
Int. J. Mol. Sci. 2023, 24(13), 11025; https://doi.org/10.3390/ijms241311025 - 03 Jul 2023
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Abstract
This study uses personalized chronic lymphoblastic leukemia (CLL) cybrid cells to test various drugs/agents designed to improve mitochondrial function and cell longevity. Age-matched control (NL) and CLL cybrids were created. The NL and CLL cybrids were treated with ibrutinib (Ibr-10 μM), mitochondrial-targeted nutraceuticals [...] Read more.
This study uses personalized chronic lymphoblastic leukemia (CLL) cybrid cells to test various drugs/agents designed to improve mitochondrial function and cell longevity. Age-matched control (NL) and CLL cybrids were created. The NL and CLL cybrids were treated with ibrutinib (Ibr-10 μM), mitochondrial-targeted nutraceuticals such as alpha lipoic acid (ALA-1 mM), amla (Aml-300 μg), melatonin (Mel-1 mM), resveratrol (Res-100 μM) alone, or a combination of ibrutinib with nutraceuticals (Ibr + ALA, Ibr + Aml, Ibr + Mel, or Ibr + Res) for 48 h. MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazoliumbromide), H2DCFDA(2′,7′ Dichlorodihydrofluorescein diacetate), and JC1 assays were used to measure the cellular metabolism, intracellular ROS levels, and mitochondrial membrane potential (∆ψm), respectively. The expression levels of genes associated with antioxidant enzymes (SOD2, GPX3, and NOX4), apoptosis (BAX and CASP3), and inflammation (IL6, IL-1β, TNFα, and TGFβ) were measured using quantitative real-time PCR (qRT-PCR). CLL cybrids treated with Ibr + ALA, Ibr + Aml, Ibr + Mel, and Ibr + Res had (a) reduced cell survivability, (b) increased ROS production, (c) increased ∆ψm levels, (d) decreased antioxidant gene expression levels, and (e) increased apoptotic and inflammatory genes in CLL cybrids when compared with ibrutinib-alone-treated CLL cybrids. Our findings show that the addition of nutraceuticals makes the CLL cybrids more pro-apoptotic with decreased cell survival compared with CLL cybrids exposed to ibrutinib alone. Full article
(This article belongs to the Special Issue Mitochondrial Metabolic Alterations in Cancer)
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Review

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15 pages, 1211 KiB  
Review
A Leukemic Target with a Thousand Faces: The Mitochondria
by Beatrice Maffeo, Cristina Panuzzo, Amedeo Moraca and Daniela Cilloni
Int. J. Mol. Sci. 2023, 24(17), 13069; https://doi.org/10.3390/ijms241713069 - 22 Aug 2023
Cited by 1 | Viewed by 1137
Abstract
In the era of personalized medicine greatly improved by molecular diagnosis and tailor-made therapies, the survival rate of acute myeloid leukemia (AML) at 5 years remains unfortunately low. Indeed, the high heterogeneity of AML clones with distinct metabolic and molecular profiles allows them [...] Read more.
In the era of personalized medicine greatly improved by molecular diagnosis and tailor-made therapies, the survival rate of acute myeloid leukemia (AML) at 5 years remains unfortunately low. Indeed, the high heterogeneity of AML clones with distinct metabolic and molecular profiles allows them to survive the chemotherapy-induced changes, thus leading to resistance, clonal evolution, and relapse. Moreover, leukemic stem cells (LSCs), the quiescent reservoir of residual disease, can persist for a long time and activate the recurrence of disease, supported by significant metabolic differences compared to AML blasts. All these points highlight the relevance to develop combination therapies, including metabolism inhibitors to improve treatment efficacy. In this review, we summarized the metabolic differences in AML blasts and LSCs, the molecular pathways related to mitochondria and metabolism are druggable and targeted in leukemia therapies, with a distinct interest for Venetoclax, which has revolutionized the therapeutic paradigms of several leukemia subtype, unfit for intensive treatment regimens. Full article
(This article belongs to the Special Issue Mitochondrial Metabolic Alterations in Cancer)
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