FOXP1 enhances tumor cell migration by repression of NFAT1 transcriptional activity in MDA-MB-231 cells.

Until now, forkhead box P1 (FOXP1) has been identified as a tumor suppressor in several correlation studies in breast cancer. Although FOXP1 is defined as a transcriptional repressor that interacts with other transcription factors in various mechanistic studies, there is no study that explains its repressor functions in breast cancer biology. This study demonstrated the repressor function of FOXP1 on nuclear factor of activated T cells (NFAT1) and the migratory effect of this repression in MDA-MB-231 breast cancer cells. Co-immunoprecipitation experiments were performed for the investigation of protein-protein interaction between two transcription factors. Protein-protein interaction on DNA was investigated with EMSA and transcriptional effects of FOXP1 on NFAT1, luciferase reporter assay was performed. Wound healing assay was used to analyze the effects of overexpression of FOXP1 on tumor cell migration. This study showed that FOXP1 has protein-protein interaction with NFAT1 on DNA and enhances breast cancer cell migration by repressing NFAT1 transcriptional activity and FOXP1 shows oncogenic function by regulating breast cancer cell motility.