<p>Bone marrow mesenchymal stem cells, also known as BMSCs, have been demonstrated to promote epithelial-to-mesenchymal transition (EMT) in triple-negative breast cancer (TNBC) cells, which contributes to the invasive and metastatic features of these cells. To be more specific, exosomes generated from bone marrow-derived mesenchymal stem cells (BMSC) that include microRNAs like miR-210-3p have the ability to activate the Wnt/β-catenin pathway, which further promotes the advancement of TNBC. Factors like as TGF-β and HGF are included in the BMSC secretome, which is a collection of chemicals that are released. These factors have the potential to contribute to extracellular matrix (ECM) and other aggressive behaviours like TNBC. Variable 2D and 3D models have been explored over the years to generate stable phenotyping characteristics of EMT in triple-negative breast cancer. Within the scope of this review, we have provided an in-depth analysis of the pathophysiology of EMT in breast cancer, as well as the varied crosstalk that occurs between distinct signalling pathways. A variety of in vivo and patient-derived xenograft models have been reviewed, along with their respective applications and possible limitations. This article provides a comprehensive discussion on the several cutting-edge 3D microphysiological disease models (Organoid, Spheroid, and Organ-on-Chip) that facilitate the replication of the pathophysiology of EMT in breast cancer. We have critically discussed our experimental observation on BMSC mediated co-conditioning and parallel cell homing with MDA-MB-231 to induce stable EMT. It will act as a marker pathway for medication targeting, treatments, and emphasis on drug resistance as a 3D in vitro microphysiological disease model.</p>