Angiotensin II (Ang II) reportedly facilitates distal hematogenous metastasis in various murine intravenous metastasis models. However, it is unclear whether Ang II accelerates the initial processes of metastasis that begins in primary tumors. We examined the effects of Ang II on primary tumors and lung metastasis lesions using a murine spontaneous metastasis model, in which triple negative breast cancer 4T1 cells were injected into the mammary fat pad of BALB/c mice. Ang II administration significantly accelerated primary tumor growth and lung metastasis formation, and Ang II type 1 receptor blocker valsartan attenuated them. Ang II increased the expression of proteins related to cell proliferation and epithelial-to-mesenchymal transition (EMT) in primary tumors, and valsartan attenuated them. However, Ang II did not change the proliferation, migration, invasion, or the protein expressions in 4T1 cells in vitro. In contrast, when 4T1 cells were co-cultured with fibroblasts, Ang II significantly accelerated cell migration and increased the expression levels of EMT-related proteins in 4T1 cells. And moreover, Ang II significantly increased the mRNA expression level of IL-6 in fibroblasts co-cultured with 4T1 cells. These results suggested that Ang II accelerates interaction between cancer cells and surrounding fibroblasts by soluble factors such as IL-6 to promote EMT and cell migration, which result in the initiation of cancer metastasis.