The entry of a cancer in its metastatic phase reduces the possibility to cure a patient. Our study tested the hypothesis of a metabolic control of metastasis, of which we identified two actors. First, using different models, we showed that mitochondrial dysfunctions associated to a non-cytotoxic increase in the production of reactive oxygen species (mtROS) promote cancer cell migration and invasion and, overall, the metastatic activity of cancer cells. We further showed that monocarboxylate transporter 1 (MCT1) triggers similar phenotypic traits by activating nuclear factor-кB (NF-кB) independently of its transport activity. Therefore, we propose mtROS inactivation with specific antioxidants targeting mitochondria (such as mitoQ and catechin:lysine 1:2) and inhibition of MCT1 expression as two complementary therapeutic strategies capable to prevent metastatic dissemination in cancer.
Payen, V. (2018). Tumor metastasis under metabolic control : characterization and potential therapeutic implications. https://hdl.handle.net/2078.5/173144