TUMOR INTRINSIC EFFECTS OF FOXP3 IN BREAST CANCER CELLS

ALEJANDRO NICOLA CANDIA; NAZARENO GONZALEZ; JORGE A. PEÑA AGUDELO; MATÍAS GARCIA FALLIT1; ANTONELA S. ASAD; SOFIA SAGRIPANTI; ARACELI ABT; MELANIE PÉREZ KÜPER; MARIELA A. MORENO AYALA; ADRIANA SEILICOVICH; FLAVIA ZANETTI; MARIANELA CANDOLFI

Mar del Plata

Otro; REUNIÓN CONJUNTA SAIC SAI&FAIC SAFIS 2022; 2022

Sociedad Argentina de Investigación Clínica

Foxp3 is a transcription factor required for Treg function. In the last years, it has been detected in breast tumor and other cancer cells, but its role in tumor pathogenesis is controversial. Our previous results suggest that P60, a cell-penetrating peptide that impairs Foxp3 function, improves the efficacy of antitumor vaccines and inhibits tumor progression in experimental breast cancer. Herewe aimed to assess the tumor intrinsic role of Foxp3 in breast cancer. Meta-analysis of Foxp3 expression in TCGA and METABRIC data bases indicated that Foxp3 is over-expressed in HER2+ and triple negative (TNBC) breast tumors compared to hormone-dependent tumors.In addition, upregulation of Foxp3 correlated with lower OS in HER2+ tumors and TNBC. Foxp3 expression positively correlated to PDL1, IDO and IL-10 expression and EMT markers. Considering that Foxp3 may affect cell survival, we next evaluated the effect of chemotherapy on its expression in HER2+ and TNBC cells. Cisplatin upregulated Foxp3 in both cell lines (p