Breast cancer (BC) is a common malignancy which is the most frequently diagnosed cancer in women all over the worldwide. This study aimed to investigate the roles of miR‐1469 in the development of BC, as well as its regulatory mechanism. The expression levels of miR‐1469 in BC tissues, serum, and cell lines were determined. Effects of overexpression of miR‐1469 on MCF7 cell viability, colony‐forming ability, apoptosis, migration, and invasion were then investigated. Furthermore, the potential target of miR‐1469 in MCF7 cells was explored. Besides, the association between miR‐1469, PTEN/PI3K/AKT, and Wnt/β‐catenin pathways was elucidated. Notably, confirmatory experiments by downregulation of miR‐1469 in SK‐BR‐3 cells were further performed. The miR‐1469 expression was significantly downregulated in BC tissues, serum, and cell lines. The overexpression of miR‐1469 significantly inhibited the proliferation, arrested cell‐cycle at G2/M phase, increased apoptosis, suppressed migration, and invasion of MCF‐7 cells. In addition, HOXA1 was verified as a direct target of miR‐1469, and the effects of overexpression of miR‐1469 on the malignant behaviors of MCF7 cells were significantly counteracted by overexpression of HOXA1 concurrently. Furthermore, the overexpression of miR‐1469 suppressed the activation of PTEN/PI3K/AKT and Wnt/β‐catenin pathways, which was reversed overexpression of HOXA1 concurrently. Besides, confirmatory experiments showed that the inhibition of miR‐1469 promoted the malignant behaviors of SK‐BR‐3 cells, which was inversed after miR‐1469 inhibition and HOXA1 knockdown at the same time. Our findings reveal that downregulation of miR‐1469 may promote the development of BC by targeting HOXA1 and activating PTEN/PI3K/AKT and Wnt/β‐catenin pathways. MiR‐1469 may serve as a promising target for BC therapy.