Placenta-specific 1 (PLAC1)， a novel cancer-testis antigen (CTA)， is expressed in a number of different human malignancies. It is frequently produced in breast cancer， serving a function in tumorigenesis. Adoptive immunotherapy using T cell receptor (TCR)-engineered T cells against CTA mediates objective tumor regression; however， to the best of our knowledge， targeting PLAC1 using engineered T cells has not yet been attempted. In the present study， the cDNAs encoding TCRα- and β-chains specific for human leukocyte antigen (HLA)-A*0201-restricted PLAC1 were cloned from a cytotoxic T-lymphocyte， generated by by the stimulation of CD8+ T cells using autologous HLA-A2+ dendritic cells loaded with a PLAC1-specific peptide (p28-36， VLCSIDWFM). The TCRα/β-chains were linked by a 2A peptide linker (TCRα-Thosea asigna virus-TCRβ)， and the constructs were cloned into the lentiviral vector， followed by transduction into human cytotoxic (CD8+) T cells. The efficiency of transduction was up to 25.16%， as detected by PLAC1 multimers. TCR-transduced CD8+ T cells， co-cultured with human non-metastatic breast cancer MCF-7 cells (PLAC1+， HLA-A2+) and triple-negative breast cancer MDAMB-231 cells (PLAC1+， HLA-A2+)， produced interferon γ and tumor necrosis factor α， suggesting TCR activation. Furthermore， the PLAC1 TCR-transduced CD8+ T cells efficiently and specifically identified and annihilated the HLA-A2+/PLAC1+ breast cancer cell lines in a lactate dehydrogenase activity assay. Western blot analysis demonstrated that TCR transduction stimulated the production of mitogen-activated protein kinase signaling molecules， extracellular signal-regulated kinases 1/2 and nuclear factor-κB， through phosphoinositide 3-kinase γ-mediated phosphorylation of protein kinase B in CD8+ T cells. Xenograft mouse assays revealed that PLAC1 TCR-transduced CD8+T cells significantly delayed the tumor progression in mice-bearing breast cancer compared with normal saline or negative control-transduced groups. In conclusion， a novel HLA-A2-restricted and PLAC1-specific TCR was identified. The present study demonstrated PLAC1 to be a potential target for breast cancer treatment; and the usage of PLAC1-specific TCR-engineered T cells may be a novel strategy for PLAC1-positive breast cancer treatment.