Updates on Mitochondria and Cancer

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: 15 January 2026 | Viewed by 920

Special Issue Editors


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Guest Editor
Department of Precision and Regenerative Medicine and Ionian Area, University of Bari, Bari, Italy
Interests: mitochondrial homeostasis (biogenesis, mitophagy and dynamics); mtDNA alterations; mitochondrial dysfunction in cancer; mitochondrial therapeutic targets in cancer
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
CNR Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies (IBIOM), Bari, Italy
Interests: mitochondrial proteome in ageing, muscle unloading and cancer; mitochondrial biogenesis; mitochondrial antioxidant proteins; mitochondrial DNA-binding proteins; mitochondrial dynamics; metabolomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria play a key role in cancer, and their involvement is not limited to ATP production. Mitochondria also produce reactive oxygen species and building blocks to support rapid cell proliferation; therefore, the deregulation of mitochondrial function is associated with the development and progression of cancer.

Metabolic reprogramming in cancer cells occurs through the modulation of mitochondrial metabolic pathways and changes in mitochondrial homeostasis (biogenesis, mitophagy, dynamics, redox balance, and protein homeostasis). A deeper understanding of altered mitochondrial pathways in cancer may provide new opportunities to identify potential therapeutic targets. In addition, several studies have shown that mitochondria are also involved in cancer drug resistance. Finally, the analysis of mitochondrial markers in cancer tissues and body fluids may provide a tool for early cancer diagnosis and the monitoring of disease progression.

Thus, this Special Issue will focus on altered mitochondrial pathways in cancer, new strategies/compounds that may induce cancer cell death by altering mitochondrial function, mitochondria and cancer drug resistance, and mitochondrial markers as new diagnostic/prognostic tools. We invite authors to submit original research and review articles related to any of these aspects.

Dr. Antonella Cormio
Dr. Clara Musicco
Guest Editors

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Keywords

  • mitochondrial dysfunction in cancer
  • mitochondrial metabolomics
  • mitochondria and cancer therapy
  • mitochondria and cancer drug resistance
  • prognostic/predictive mitochondrial markers in cancer tissues and body fluids

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Published Papers (1 paper)

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Research

25 pages, 4338 KB  
Article
Mitochondrial Dysfunction in Apoptosis-Resistant Acute Myeloid Leukemia Cells During a Sterile Inflammatory Response
by Elena I. Meshcheriakova, Kirill S. Krasnov, Irina V. Odinokova, Aleksey I. Lomovsky, Olga V. Krestinina, Yuliya L. Baburina, Irina B. Mikheeva, Gulnara Z. Mikhailova, Anatoly S. Senotov, Polina S. Nekhochina, Yana V. Lomovskaya, Vladislav V. Minaychev, Irina S. Fadeeva, Margarita I. Kobyakova and Roman S. Fadeev
Biomolecules 2025, 15(12), 1635; https://doi.org/10.3390/biom15121635 - 21 Nov 2025
Viewed by 609
Abstract
Mitochondria are crucial for energy metabolism and the regulation of apoptosis and the inflammatory response in acute myeloid leukemia (AML). This study examined key mitochondrial characteristics in apoptosis-resistant AML cells during in vitro aseptic pro-inflammatory activation utilizing spectrofluorimetry, quantitative reverse transcription PCR, Western [...] Read more.
Mitochondria are crucial for energy metabolism and the regulation of apoptosis and the inflammatory response in acute myeloid leukemia (AML). This study examined key mitochondrial characteristics in apoptosis-resistant AML cells during in vitro aseptic pro-inflammatory activation utilizing spectrofluorimetry, quantitative reverse transcription PCR, Western blotting, differential gene expression analysis, flow cytometry, transmission electron microscopy, and cellular respiration analysis. Under conditions of aseptic inflammation simulated in three-dimensional high-density cultures, apoptosis-resistant AML cells exhibited a significant reduction in the transcriptional activity of genes linked to oxidative phosphorylation and the tricarboxylic acid cycle; demonstrated diminished mitochondrial respiration activity; and decreased levels of the mitophagy regulatory proteins PINK1 and Parkin. Furthermore, pathogenic alterations in mitochondrial morphology were observed. These cells demonstrated enhanced intracellular generation of reactive oxygen species, lactate accumulation in the culture media, elevated levels of DRP1 protein, and an increased fraction of small and medium-sized mitochondria. The acquired data demonstrate that aseptic pro-inflammatory activation results in metabolic remodelling of acute myeloid leukemia cells, integrating characteristics of mitochondrial dysfunction. This condition may facilitate the persistence of leukemic cells during inflammatory stress and potentially contribute to the development of an apoptosis-resistant phenotype. The established in vitro model is crucial for examining both the characteristics of energy metabolism and the anti-apoptotic mechanisms in leukemic cells. Full article
(This article belongs to the Special Issue Updates on Mitochondria and Cancer)
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