Mitochondrial Redox Hubs as Promising Targets for Anticancer Therapy

Mitochondria play multifaceted roles in malignant tumor progression. Beyond their bioenergetic role, mitochondria are essential for providing malignant cells a higher plasticity to face the harsh environmental conditions. Cell-autonomous metabolic deregulation of cancer cells, or metabolic adaptatio...

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Published inFrontiers in oncology Vol. 10; p. 256
Main Authors Ippolito, Luigi, Giannoni, Elisa, Chiarugi, Paola, Parri, Matteo
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 28.02.2020
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Summary:Mitochondria play multifaceted roles in malignant tumor progression. Beyond their bioenergetic role, mitochondria are essential for providing malignant cells a higher plasticity to face the harsh environmental conditions. Cell-autonomous metabolic deregulation of cancer cells, or metabolic adaptation to microenvironmental cues (lack of nutrients, stromal supply, hypoxia, etc.), represent the triggering event of mitochondria overexploitation to orchestrate nutrient sensing and upload, signaling, and redox circuits. As readout of their higher function, mitochondria produce high amounts of reactive oxygen species (ROS) that are functional for multiple signaling networks underlying tumor proliferation, survival, and metastatic process. To compensate for the higher rate of mitochondrial ROS production, cancer cells have evolved adaptive mechanisms to increase their antioxidant systems and to address ROS activating pathways useful for the tumor cell adaptation to environmental changes. As these properties are critical for cancer progression, mitochondrial ROS have recently become an attractive target for anti-cancer therapies. We discuss how understanding of mitochondrial function in the tumor-specific generation of ROS will impact on the development of novel redox-based targeted therapeutic strategies.
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This article was submitted to Cancer Metabolism, a section of the journal Frontiers in Oncology
Reviewed by: Nadège Bellance, Université de Bordeaux, France; Katarína Smolková, Institute of Physiology (ASCR), Czechia
Edited by: Yong Teng, Augusta University, United States
ISSN:2234-943X
2234-943X
DOI:10.3389/fonc.2020.00256