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Epithelial‐to‐mesenchymal transition (EMT), driven by cues from the tumor microenvironment, is a critical initiator of metastatic progression. In breast cancer patients, elevated expression of cartilage oligomeric matrix protein (COMP) is associated with shorter survival and increased metastatic risk. Here, we investigated the role of COMP in regulating EMT in breast cancer. Breast cancer cells treated with recombinant COMP or engineered to overexpress COMP exhibited a marked decrease in the epithelial marker CDH1 and an increase in mesenchymal markers such as VIM and VCAN. Consistent with these in vitro findings, COMP‐expressing xenograft tumor tissues showed enhanced EMT characteristics. Functionally, COMP promoted increased migration and invasion of breast cancer cells in both autocrine and paracrine manners, dependent on its thrombospondin (TSP) and C‐terminal domains. We further identified protein TMEPAI (encoded by gene PMEPA1) as a functional COMP‐binding partner that mediates COMP‐induced EMT, primarily through interaction with the TSP domain of COMP. Mechanistically, COMP shifted transforming growth factor beta (TGFβ) signaling from canonical phosphorylated mothers against decapentaplegic homolog 2/3 (pSMAD2/3) activation toward pSMAD1/5, likely through its interaction with PMEPA1. This study suggests the COMP–PMEPA1 axis as a new driver of EMT in breast cancer models. This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.