<p>Breast cancer (BC) remains the most prevalent malignancy among women and a leading cause of cancer-related mortality worldwide. Despite significant advances in recent decades, the molecular mechanisms underlying BC pathogenesis are not yet fully elucidated. Emerging evidence indicates that more than half of the members of the tripartite motif (TRIM) protein superfamily, the majority of which exhibit E3 ubiquitin ligase activity, contribute to BC initiation, progression, and metastasis by exerting functions as either oncoproteins or tumor suppressors. TRIM proteins participate in diverse cellular processes and signaling pathways. In this review, we discuss the specific molecular mechanisms by which TRIM proteins influence BC development, including post-transcriptional modifications, regulation of apoptosis and autophagy, cell cycle control, and metabolic reprogramming of glucose and lipid pathways. A notable feature of TRIM proteins is their engagement in diverse cellular processes and signaling pathways, coupled with their ability to play opposing roles – either promoting or inhibiting BC development – thus reflecting a ‘yin and yang’ paradigm. Collectively, current data suggest that <i>TRIM</i> genes and their protein products represent promising targets for therapeutic intervention and potential biomarkers for BC prognosis and disease progression.</p> Graphical abstract <p></p>