<b>A lactate-fatty acid loop drives prostate cancer bone colonization by mediating metabolic interplay between tumor cells and osteoblasts</b>

However, current frontline treatments offer only marginal improvements in survival and symptom management. In this study, we investigated the metabolic landscape of BoM lesions of PCa and found that prostate tumors rewire their metabolism to adapt to the bone microenvironment, utilizing lactate as an alternative nutrient source.

Beyond its previously reported role in oxidative phosphorylation (OXPHOS), lactate serves as a net carbon source for fatty acid synthesis (FAS) in bone-colonized cancer cells. In turn, these cancer cells produce oleic acid (OA), which enhances osteoblast activity and drives pathological osteogenesis. At the molecular level, we identified monocarboxylate transporter 1 (MCT1) as the key membrane transporter enabling prostate tumor cells to take up lactate from the bone microenvironment.