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Obesity has reached a pandemic proportion and is responsible for the augmentation of multimorbidity including certain cancers. With the rise in obesity amongst the female population globally, a concomitant increase in breast cancer (BC) incidence and related mortality has been observed. In the present review, we have elucidated the cellular and molecular insight into the visfatin-mediated cellular plasticity programs such as Epithelial to mesenchymal transition (EMT) and Endothelial to mesenchymal transition (EndoMT), and stemness-associated changes in BC cells. EMT and EndoMT are responsible for inducing metastasis in cancer cells and conferring chemotherapy resistance, immune escape, and infinite growth potential. Visfatin, an obesity-associated adipokine implicated in metabolic syndrome, has emerged as a central player in BC pathogenesis. Several studies have indicated the presence of visfatin in the tumor microenvironment (TME) where it augments EMT and EndoMT of BC cells. Further, Visfatin also modulates the TME by acting on the tumor stroma cells such as adipocytes, infiltrated immune cells, and adipose-associated stem cells that secrete factors such as cytokines, and extracellular vesicles responsible for augmenting cellular plasticity program. Visfatin induced altered metabolism of the cancer cells and molecular determinants such as non-coding RNAs involved in EMT and EndoMT have been discussed. We have also highlighted specific therapeutic targets that can be exploited for the development of effective BC treatment. Taken together, these advanced understandings of cellular and molecular insight into the visfatin-mediated cellular plasticity programs may stimulate the development of better approaches for the prevention and therapy of BC, especially in obese patients.