Non-coding RNAs play essential roles in
breast cancer progression by regulating proliferation, differentiation, invasion, and
metastasis. However, our understanding of most
microRNAs (
miRNAs) and long noncoding RNAs (lncRNAs) in
breast cancer is still limited. miR-586 has been identified as an important factor in the progression of some types of
cancer, but its exact function and relative regulation mechanisms in
breast cancer development need to be further investigated. In this study, we showed miR-586 functioned as an oncogene by promoting
breast cancer proliferation and
metastasis both in vitro and in vivo. Meanwhile, miR-586 induced Wnt/β-
catenin activation by directly targeting Wnt/β-
catenin signaling antagonists SFRP1 and DKK2/3. Moreover, we demonstrated that LINC01189 functioned as a
tumor suppressor and inhibited
breast cancer progression through inhibiting an epithelial-mesenchymal transition (EMT)-like phenotype by sponging miR-586. In addition, β-
catenin/TCF4 transactivated ZEB1, resulting in a transcriptional repression of LINC01189 expression. In conclusion, our data uncovered the LINC01189-miR-586-ZEB1 feedback loop and provided a novel mechanism participating in the regulation of Wnt/β-
catenin signaling in
breast cancer progression.