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Role of Mitochondria in Cancer

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

Deadline for manuscript submissions: 20 May 2025 | Viewed by 1509

Special Issue Editors


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Guest Editor
Division of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan
Interests: p53; tumor suppressor; phase-separation; droplets; membrane-less organelles; cardiolipin metabolism; mitochondrial quality control; apoptosis; cancer metabolism

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Guest Editor
Department of Health Sciences, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
Interests: mitochondria; lysosome; drug resistance; cancer stem; glioblastoma; translation; ferroptosis; cancer metabolism

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Guest Editor
Department of Breast Surgery, Gifu University Hospital, 1-1 Yanagido, Gifu 501-1194, Japan
Interests: surgical oncology; breast cancer; GI cancer; tumor suppressor; cancer metabolism; molecular target drug; translational research; prognostic factor

Special Issue Information

Dear Colleagues,

In healthy cells, mitochondria are essential for producing ATP efficiently via respiration, but in pathological situations, they may trigger apoptosis by releasing cytochrome c; thus, they serve critical functions in both cell survival and death. Mitochondria are also central to cellular metabolism. Nearly 100 years ago, Otto Warburg opined, “The mitochondria of cancer cells are abnormal”. He observed that cancer cells predominantly depend on glycolytic energy production, even though they exist in aerobic conditions. Since then, a number of studies have reported mitochondrial dysregulation and dysfunction in cancer cells. However, how and why these abnormal mitochondria contribute to cancer initiation and progression is not entirely clear. This Special Issue seeks to clarify the full picture of mitochondria in cancer. For this purpose, we invite both original and review articles on cancer mitochondria from perspectives of mitochondrial DNA/RNA, proteins, metabolism, apoptosis, oxidative stress, proteostasis, autophagy, lipid, fission and fusion, and droplets. This Special Issue also welcomes both basic and translational research on molecular bases and pathophysiology of cancer mitochondria, and therapeutic and diagnostic applications of dysfunctional mitochondria in cancer.

Prof. Dr. Hirofumi Arakawa
Prof. Dr. Takeshi Uchiumi
Dr. Manabu Futamura
Guest Editors

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Keywords

  • metabolism
  • apoptosis
  • fusion and fission
  • mitochondrial DNA
  • mitochondrial RNA
  • mitochondrial proteins
  • mitophagy
  • lipid
  • cardiolipin
  • phase separation
  • oxidative phosphorylation
  • proteostasis
  • mitochondrial quality control
  • TFAM
  • anti-cancer drug
  • imaging
  • cancer therapy
  • cancer diagnosis
  • Warburg effect

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Published Papers (1 paper)

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Review

26 pages, 2018 KiB  
Review
Mitochondrial Plasticity and Glucose Metabolic Alterations in Human Cancer under Oxidative Stress—From Viewpoints of Chronic Inflammation and Neutrophil Extracellular Traps (NETs)
by Hui-Ting Lee, Chen-Sung Lin, Chao-Yu Liu, Po Chen, Chang-Youh Tsai and Yau-Huei Wei
Int. J. Mol. Sci. 2024, 25(17), 9458; https://doi.org/10.3390/ijms25179458 - 30 Aug 2024
Viewed by 1084
Abstract
Oxidative stress elicited by reactive oxygen species (ROS) and chronic inflammation are involved both in deterring and the generation/progression of human cancers. Exogenous ROS can injure mitochondria and induce them to generate more endogenous mitochondrial ROS to further perpetuate the deteriorating condition in [...] Read more.
Oxidative stress elicited by reactive oxygen species (ROS) and chronic inflammation are involved both in deterring and the generation/progression of human cancers. Exogenous ROS can injure mitochondria and induce them to generate more endogenous mitochondrial ROS to further perpetuate the deteriorating condition in the affected cells. Dysfunction of these cancer mitochondria may possibly be offset by the Warburg effect, which is characterized by amplified glycolysis and metabolic reprogramming. ROS from neutrophil extracellular traps (NETs) are an essential element for neutrophils to defend against invading pathogens or to kill cancer cells. A chronic inflammation typically includes consecutive NET activation and tissue damage, as well as tissue repair, and together with NETs, ROS would participate in both the destruction and progression of cancers. This review discusses human mitochondrial plasticity and the glucose metabolic reprogramming of cancer cells confronting oxidative stress by the means of chronic inflammation and neutrophil extracellular traps (NETs). Full article
(This article belongs to the Special Issue Role of Mitochondria in Cancer)
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