Exit of quiescent disseminated cancer cells from dormancy is thought to be responsible for metastatic relapse and a better understanding of dormancy could pave the way for novel therapeutic approaches. We used anin vivomodel of triple negative breast cancer brain metastasis to identify differences in transcriptional profiles between dormant and proliferating cancer cells in the brain.BGNgene, encoding a small proteoglycan biglycan, was strongly upregulated in dormant cancer cellsin vivo.BGNexpression was significantly downregulated in patient brain metastases as compared to the matched primary breast tumors andBGNoverexpression in cancer cells inhibited their growthin vitroandin vivo. Dormant cancer cells were further characterized by a reduced expression of glycolysis genesin vivo, and inhibition of glycolysisin vitroresulted in a reversible growth arrest reminiscent of dormancy. Our study identified mechanisms that could be targeted to induce/maintain cancer dormancy and thereby prevent metastatic relapse.