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Mitochondria: Central Players in Cancer

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

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1034

Special Issue Editors


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Guest Editor
Department of Clinical and Experimental Medicine, University of Foggia, Via Pinto 1, 71122 Foggia, Italy
Interests: mitochondria; mitochondrial dysfunction; oxidative phosphorylation; tumorigenesis; cancer therapy

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy
Interests: cancer biology and therapy; angiogenesis/anti-angiogenesis; chemoprevention
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Special Issue Information

Dear Colleagues,

Mitochondria, the energy centers of cells, are intrinsically involved in cancer development. Beyond energy production, they regulate vital processes such as cell death. In cancer, mitochondrial function is often disrupted, leading to metabolic shifts favoring increased glycolysis (the Warburg effect), the increased production of harmful reactive oxygen species (ROS), and resistance to programmed cell death (apoptosis). These alterations contribute significantly to cancer progression. The focus of this Special Issue will be on exploring the role of mitochondria in the progression of carcinogenesis and identifying novel potential therapeutic strategies for cancer treatment by targeting mitochondrial function.

Dr. Annamaria Piscazzi
Dr. Domenica Mangieri
Guest Editors

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Keywords

  • mitochondria
  • cancer
  • tumorigenesis
  • oxidative phosphorylation
  • glycolysis
  • Warburg effect
  • reactive oxygen species (ROS)
  • apoptosis
  • mitochondrial dysfunction
  • metabolic reprogram-ming
  • cancer therapy

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Published Papers (1 paper)

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Research

18 pages, 2970 KiB  
Article
Gα13 Promotes Clonogenic Growth by Increasing Tolerance to Oxidative Metabolic Stress in Prostate Cancer Cells
by Di Wu, Wei Kiang Lim, Xiaoran Chai, Veerabrahma Pratap Seshachalam, Suhail Ahmed Kabeer Rasheed, Sujoy Ghosh and Patrick J. Casey
Int. J. Mol. Sci. 2025, 26(10), 4883; https://doi.org/10.3390/ijms26104883 - 20 May 2025
Viewed by 143
Abstract
The oncogenic role of the G12 family in many human solid cancers has been extensively studied, primarily through the effects of constitutively active mutants of these proteins on cell migration and invasion. However, these mutations are not seen in cancers, and the biological [...] Read more.
The oncogenic role of the G12 family in many human solid cancers has been extensively studied, primarily through the effects of constitutively active mutants of these proteins on cell migration and invasion. However, these mutations are not seen in cancers, and the biological role of Gα13 in prostate cancer tumorigenesis is largely unexplored. Here, we report that Gα13 promotes anchorage-independent colony formation, spheroid formation, and xenograft tumor growth in human prostate cancer cell lines. Transcriptome analyses suggest that Gα13 modulates genes in the mitochondria and are involved in the oxidative stress response. Silencing of GNA13 increased mitochondrial superoxide levels when prostate cancer cells were cultured in galactose medium and increased the sensitivity to oxidative metabolic stress when the cells were cultured in media containing non-glycolytic metabolites. Furthermore, Gα13 levels impacts the abundance of superoxide dismutase 2 (SOD2) in the mitochondria, as well as SOD2 promoter activity and mRNA expression. Importantly, expression of SOD2 could rescue the effect of Gα13 loss on suppression of anchorage-independent growth. Likewise, stable knockdown of SOD2 decreased anchorage-independent cell growth, which was enhanced by overexpression of Gα13. These results outline a novel biological function of Gα13 mediated via SOD2 in prostate cancer tumorigenesis and highlight it as a potential treatment target. Full article
(This article belongs to the Special Issue Mitochondria: Central Players in Cancer)
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