Low miR-96-5p expression is characteristic of many cancers but its role in breast cancer (BCa) remains poorly defined. Here, the role of miR-96-5p in BC development was assessed. We demonstrate that exogenously expressing miR-96-5p inhibits the proliferative, migratory and invasive capacity of BCa cells. Mechanistically, miR-96-5p in BCa cells was found to target and downregulate catenin delta 1 (CTNND1) leading to decreased β-catenin expression, a loss of WNT11 signaling, reduced cyclin D1 levels and lower MMP7 expression. Exogenously expressing CTNND1 alleviated these effects. In summary, we are the first to reveal that miR-96-5p inhibits the proliferative, invasive and migratory phenotypes of BCa cells the targeting of CTNND1 and subsequent Wnt/β-catenin signaling. These data highlight miR-96-5p as a novel target for BC treatment. Of all life-threatening human cancer cases, breast cancer (BCa) remains the most commonly diagnosed 1. In the United States (US), nearly 330,000 new cases of BC occurred in 2017 over a third of which were invasive 2. Despite great strides to improve BCa diagnostics and therapeutics, the rates of mortality remain high with over 40000 deaths occurring in 2017 in the US alone 2. BCa cells possess a remarkable ability to metastasize to the bone marrow, the regional lymph nodes, liver, and the lungs forming a distinct tissue microenvironment (TME) that permits efficient dissemination from the site of the primary tumor 3,4. Identifying the molecular mechanisms controlling BCa progression can thus inform the design of more efficacious anti-BCa therapies. It is now well-accepted that the dysregulation of cellular MicroRNAs (miRNAs) leads to a range of pathological processes in animals and humans mediated through their ability to bind protein-coding transcripts 5. An increasing body of evidence points to the presence of a link between miRNAs to the initiation, development, and metastasis of various types of tumors, including BC 6-9. Although miR-96-5p is implicated in multiple cancers 10-12 , little is known regarding its relationship to the development and progression of BC. Here, we assessed the contribution of miR-96-5p to BCa and reveal its downregulation in BCa cells. We demonstrate that exogenously increasing miRNA-95-5p expression inhibits the proliferative and metastatic potential of BCa cells which is in part, mediated through the targeting of catenin delta 1 (CTNND1) and subsequent Wnt/β-catenin signaling. We thus highlight miR-96-5p as a novel therapeutic for much needed anti-BCa treatments. Methods Tissues and cells. We collected 155 BCa samples and non-tumor tissues. Included patients received no prior chemotherapy, immunotherapy, or radiotherapy prior to the surgery. Samples were verified as BCa for an experienced pathologist and frozen in liquid N2 prior to use. All patients signed an informed consent form. The protocol of the study was reviewed and approved by the Institutional Human Experiment and Ethic Committee of the First Affiliated Hospital of Henan University of Science...