Inflammation and hypoxia are known to promote the metastatic progression of tumours. The CCAAT/enhancer‐binding protein‐δ (C/EBPδ, CEBPD) is an inflammatory response gene and candidate tumour suppressor, but its physiological role in tumourigenesis in vivo is unknown. Here, we demonstrate a tumour suppressor function of C/EBPδ using transgenic mice overexpressing the Neu/Her2/ERBB2 proto‐oncogene in the mammary gland. Unexpectedly, this study also revealed that C/EBPδ is necessary for efficient tumour metastasis. We show that C/EBPδ is induced by hypoxia in tumours in vivo and in breast tumour cells in vitro, and that C/EBPδ‐deficient cells exhibit reduced glycolytic metabolism and cell viability under hypoxia. C/EBPδ supports CXCR4 expression. On the other hand, C/EBPδ directly inhibits expression of the tumour suppressor F‐box and WD repeat‐domain containing 7 gene (FBXW7, FBW7, AGO, Cdc4), encoding an F‐box protein that promotes degradation of the mammalian target of rapamycin (mTOR). Consequently, C/EBPδ enhances mTOR/AKT/S6K1 signalling and augments translation and activity of hypoxia‐inducible factor‐1α (HIF‐1α), which is necessary for hypoxia adaptation. This work provides new insight into the mechanisms by which metastasis‐promoting signals are induced specifically under hypoxia.