Subclinical dose irradiation triggers human breast cancer migration via mitochondrial reactive oxygen species

Despite technological advances in radiotherapy, cancer cells at the tumor margin and in diffusive infiltrates can receive subcytotoxic doses of photons. Even if only a minority of cancer cells are concerned, phenotypic consequences could be important considering that mitochondrial DNA (mtDNA) is a p...

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Bibliographic Details
Published in:Cancer & metabolism 2024-07, Vol.12 (1), p.20-11, Article 20
Main Authors: Rondeau, Justin D, Van de Velde, Justine A, Bouidida, Yasmine, Sonveaux, Pierre
Format: Article
Language:English
Subjects:
Apoptosis
Breast cancer
Brief Report
Cancer therapies
Cell adhesion & migration
DNA binding proteins
Drug dosages
Genes
Genetic transcription
Glucose
Kinases
Metastasis
Migration
Mitochondria
Mitochondrial DNA
MitoQ
Oximetry
Protocol
Radiation
Radiation therapy
Reactive oxygen species
Reactive oxygen species (ROS)
Subclinical dose irradiation
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Summary:Despite technological advances in radiotherapy, cancer cells at the tumor margin and in diffusive infiltrates can receive subcytotoxic doses of photons. Even if only a minority of cancer cells are concerned, phenotypic consequences could be important considering that mitochondrial DNA (mtDNA) is a primary target of radiation and that damage to mtDNA can persist. In turn, mitochondrial dysfunction associated with enhanced mitochondrial ROS (mtROS) production could promote cancer cell migration out of the irradiation field in a natural attempt to escape therapy. In this study, using MCF7 and MDA-MB-231 human breast cancer cells as models, we aimed to elucidate the molecular mechanisms supporting a mitochondrial contribution to cancer cell migration induced by subclinical doses of irradiation (
ISSN:2049-3002
2049-3002
DOI:10.1186/s40170-024-00347-1