TGF‐β signaling pathway plays a key role in breast cancer metastasis. Recent studies suggest that TGF‐β regulates tumor progression and invasion not only via transcriptional regulation, but also via translational regulation. Using both bioinformatics and experimental tools, we identified a micropeptide CIP2A‐BP encoded by LINC00665, whose translation was downregulated by TGF‐β in breast cancer cell lines. Using TNBC cell lines, we showed that TGF‐β‐activated Smad signaling pathway induced the expression of translation inhibitory protein 4E‐BP1, which inhibited eukaryote translation initiation factor elF4E, leading to reduced translation of CIP2A‐BP from LINC00665. CIP2A‐BP directly binds tumor oncogene CIP2A to replace PP2A's B56γ subunit, thus releasing PP2A activity, which inhibits PI3K/AKT/NFκB pathway, resulting in decreased expression levels of MMP‐2, MMP‐9, and Snail. Downregulation of CIP2A‐BP in TNBC patients was significantly associated with metastasis and poor overall survival. In the MMTV‐PyMT model, either introducing CIP2A‐BP gene or direct injection of CIP2A‐BP micropeptide significantly reduced lung metastases and improved overall survival. In conclusion, we provide evidence that CIP2A‐BP is both a prognostic marker and a novel therapeutic target for TNBC.