Breast cancer (BC) is a common malignancy worldwide. More than 3 700 000 women die of BC every year. DSCAM‐AS1 was overexpressed several kinds of cancer and miR‐204‐5p was lowly expressed, which indicated that miR‐204‐5p had anti‐tumor activity and DSCAM‐AS1 had pro‐tumor activity. We intended to analyze DSCAM‐AS1, miR‐204‐5p, and ribonucleotide reductase M2 (RRM2). Microarray analysis and quantitative Real Time fluorescence Polymerase Chain Reaction (qRT‐PCR) were employed to determine DSCAM‐AS1 and miR‐204‐5p expression. Luciferase reporter assay was applied to examine the target relationship between DSCAM‐AS1, miR‐204‐5p, and RRM2. Cell Counting Kit‐8 (CCK‐8 assay), transwell assay, and flow cytometry were used to detect cell proliferation, invasion, and apoptosis. The expression of DSCAM‐AS1, miR‐204‐5p, and RRM2 were confirmed by Western blot. We also conducted in vivo assay to verify the effect of DSCAM‐AS1. DSCAM‐AS1 was up‐regulated, while miR‐204‐5p was down‐regulated in BC tissues and cells. DSCAM‐AS1 directly targeted miR‐204‐5p. DSCAM‐AS1 promoted the proliferation and invasion of BC cells by reducing miR‐204‐5p and inhibiting miR‐204‐5p expression. DSCAM‐AS1 expression was related to the expression of RRM2, and miR‐204‐5p could reverse the function of DSCAM‐AS1. RRM2 was up‐regulated in BC cells, and miR‐204‐5p inhibited RRM2 expression by targeting RRM2. Overexpression of RRM2 stimulated proliferation and cell invasion and impeded apoptosis. In vivo experiments showed that knockdown of DSCAM‐AS1 decreased the tumorigenesis of BC cells, increased the expression of miR‐204‐5p. DSCAM‐AS1 promoted proliferation and impaired apoptosis of BC cells by reducing miR‐204‐5p and enhancing RRM2 expression. DSCAM‐AS1/miR‐204‐5p/RRM2 may serve as novel therapeutic targets for BC.