Tumor-infiltrating lymphocytes are associated with [Formula: see text]-catenin overexpression in breast cancer

BACKGROUND: Inhibition of lymphocytes infiltration and activity may impair antitumor immune response and limit treatment responsiveness. Wnt/ [Formula: see text]-catenin pathway has been suggested to contribute to immune evasion in tumor by suppressing the function of immune cells and excluding T cell infiltration. However, the effects of Wnt/ [Formula: see text]-catenin on TILs recruitment remain controversial. OBJECTIVE: We aimed to investigate whether intratumoral Wnt/ [Formula: see text]-catenin signaling could affect the lymphocyte infiltration in breast cancer. METHODS: The distribution of stromal TILs, CD8 [Formula: see text] and FOXP3 [Formula: see text] TIL subsets, and the expression of [Formula: see text]-catenin were separately assessed on consecutive sections of 96 breast cancer specimens. RESULTS: Both stromal infiltrated TILs and [Formula: see text]-catenin expression were upregulated in hormone receptor negative HER2-enriched and TNBC subtypes. Furthermore, high levels of stromal TILs as well as CD8 [Formula: see text] or FOXP3 [Formula: see text] TIL subsets were associated with [Formula: see text]-catenin overexpression by breast cancer, respectively. CONCLUSIONS: For the first time, we demonstrated that rather than excluding lymphocytes infiltration as reported in mela-noma, high levels of TILs were associated with [Formula: see text]-catenin overexpression in BC. Wnt/ [Formula: see text]-catenin signaling may play a critical role in BC immunity, particularly in HER2-enriched and triple negative BC, and may serve as a potential target for regulating immune infiltrates in breast cancer.