Here, we sought to determine: 1) whether breast cancer cells can induce a loss of Cav1 and a gain of MCT4 in normal adjacent fibroblasts; 2) whether this system affects the secretion of TGFβ, IL-6, and lactate; 3) whether this new phenotype is modulated by metformin; and 4) whether mitochondrial inhibition (OXPHOS) by metformin can reduce tumor proliferation in a mouse model of breast cancer. This evidence concerns the gene CAV1 and breast carcinoma.