mtDNA and Mitochondrial Stress Signaling in Cancers

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (25 October 2023) | Viewed by 1608

Special Issue Editors

Department of Radiotherapy, Medical University in Lublin, Chodźki 7, 20-093 Lublin, Poland
Interests: cancers treatment; chemotherapy; immunotherapy; mitochondrial DNA
Special Issues, Collections and Topics in MDPI journals
Institute of Biological Bases of Animal Production, University of Life Sciences in Lublin, Akademicka 13, 20-950 Lublin, Poland
Interests: mtDNA, carcinogenesis; animal and human genetics and genomics

Special Issue Information

Dear Colleagues,

To date, the role of mitochondria and changes in mitochondrial DNA in carcinogenesis are perceived as complex and not fully understood. Most of the mtDNA somatic mutations in tumors have been also reported as polymorphisms in the general population. Numerous researchers have indicated a relationship between the occurrence of polymorphisms in mtDNA and an increased risk of cancer, including breast or prostate cancer. Their position in a given mitochondrial haplogroup may not only promote the development of cancer, but also protect against its occurrence.

Clinical manifestation of changes in mtDNA may occur as a result of the coexistence and interaction of various external and internal factors. Thus, the coexistence of mitochondrial polymorphisms may contribute to cell energy disturbances and promote the formation of cancers.

The mitochondria of cancer cells have the ability to adapt to both metabolic and oxidative stress. Mitochondrial stress response mitigation via signaling pathways maintains mitochondrial integrity. Maintaining the integrity of the mitochondria in the stress response is one of the reasons for the progression and resistance of tumors to treatment. Research on mtDNA, as well as the signaling pathways that affect mitochondrial stability, may contribute to a better understanding of the carcinogenesis processes, and thus to the introduction of new anti-cancer therapies.

Potential topics include, but are not limited to, the following:

  1. Polymorphism and mutations of mtDNA in tumors.
  2. Oxydative phosphorylation in tumors.
  3. Signaling pathways and mitochondrias in tumors.
  4. Mitochondrial metabolism in tumors.
  5. Mitochondria and metabolic or oxydative stress.

Dr. Ludmiła Grzybowska-Szatkowska
Prof. Dr. Brygida Ślaska
Guest Editors

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Keywords

  • mtDNA
  • signaling pathways
  • oxidative stress
  • mitochondria
  • carcinogenesis

Published Papers (1 paper)

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Research

15 pages, 1447 KiB  
Article
Mutations in Structural Genes of the Mitochondrial Complex IV May Influence Breast Cancer
by Ricardo Cunha de Oliveira, Sávio Pinho dos Reis and Giovanna C. Cavalcante
Genes 2023, 14(7), 1465; https://doi.org/10.3390/genes14071465 - 18 Jul 2023
Viewed by 1284
Abstract
Although it has gained more attention in recent years, the relationship between breast cancer (BC) and mitochondrial oxidative phosphorylation (OXPHOS) is still not well understood. Importantly, Complex IV or Cytochrome C Oxidase (COX) of OXPHOS is one of the key players in mitochondrial [...] Read more.
Although it has gained more attention in recent years, the relationship between breast cancer (BC) and mitochondrial oxidative phosphorylation (OXPHOS) is still not well understood. Importantly, Complex IV or Cytochrome C Oxidase (COX) of OXPHOS is one of the key players in mitochondrial balance. An in silico investigation of mutations in structural genes of Complex IV was conducted in BC, comprising 2107 samples. Our findings show four variants (rs267606614, rs753969142, rs199476128 and rs267606884) with significant pathogenic potential. Moreover, we highlight nine genes (MT-CO1, MT-CO2, MT-CO3, CO4I2, COX5A, COX5B, COX6A2, COX6C and COX7B2) with a potential impact on BC. Full article
(This article belongs to the Special Issue mtDNA and Mitochondrial Stress Signaling in Cancers)
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