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This study investigated whether the vitamin D receptor (VDR) modulates aggressiveness and chemotherapeutic response in TNBC and explored its interaction with paclitaxel (PTX) in the presence of a non\u2010hypercalcemic vitamin D analogue (UVB1). Functional cellular assays, orthotopic murine models, and computational approaches were integrated using murine 4T1 and human MDA\u2010MB\u2010468 TNBC cells with differential VDR expression, including PTX\u2010resistant models. The results show that VDR overexpression reduced invasive capacities in vitro and pulmonary metastatic dissemination in vivo, and sensitized cells to PTX alone or combined with UVB1. 4T1\u2010PTX\u2010resistant cells exhibited elevated VDR levels and less aggressive features compared with wild\u2010type cells. Computational analyses revealed stable PTX binding to an allosteric site near the activation function\u20102 domain of VDR, further stabilized by UVB1. 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