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

ABSTRACT:

Background

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 d

SUBMITTER: Rondeau JD 

PROVIDER: S-EPMC11229245 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature