We find that lncRNA ANCR participates in TGF-B1-induced EMT. By our ChIP and Real-time PCR assays, we reveal that TGF-B1 down-regulates ANCR expression by increasing HDAC3 enrichment at ANCR promoter region, which decreases both H3 and H4 acetylation of ANCR promoter. In addition, by western blot and transwell assays, we indicate that ectopic expression of ANCR partly attenuates the TGF-B1-induced EMT. Downstream, ANCR inhibits breast cancer cell migration and breast cancer metastasis by decreasing RUNX2 expression in vitro and in vivo. Thus, our study identifies ANCR, as a new TGF-B downstream molecular, is essential for TGF-B1-induced EMT by decreasing RUNX2 expression. These results implicate that ANCR might become a prognostic biomarker and an anti-metastasis therapy target for breast cancer. These results demonstrate that ANCR is down-regulated during the TGF-B1-induced EMT in MCF10A cells.