CUT&Tag profiling of SYCP1 genomic occupancy in MCF7 breast cancer adenocarcinoma cells upon SYCP1 overexpression
Through various approaches we demonstrate that SYCP1 is aberrantly re-expressed in tumor cells, where it actively promotes DNA damage repair, cell cycle progression, and malignant growth. SYCP1 binds chromatin at regulatory elements and directly controls transcriptional programs governing genome maintenance, including key effectors such as CCNB1, PCNA, RAD51C, and H2AX. Loss of SYCP1 impairs DNA repair kinetics, attenuates tumor cell proliferation and migration, and increases sensitivity to chemotherapeutics cisplatin and gemcitabine. Mechanistically, SYCP1 interfaces with chromatin remodeling complexes and transcription factors SP1 and SP2, modulating their genomic occupancy and facilitating oncogenic transcriptional outputs. Our findings illuminate a previously unrecognized moonlighting function of SYCP1 in somatic cancer cells and position it as a critical chromatin-associated regulator of genome stability. In the presented CUT&Tag experiment, we aimed to identify the genomic loci occupied by SYCP1 protein upon its overexpression in MCF7 cells.