Researchers at the University of Liverpool have discovered that SYCP1, a protein previously thought to function only during the production of sperm and eggs, can be reactivated in cancer cells where it helps tumours survive and grow.
The study, published in Science Advances, reveals that SYCP1 switches from its normal reproductive role to an entirely different function in cancer. Instead of helping chromosomes pair during meiosis, the protein enters the nucleus of cancer cells, binds directly to DNA, and controls genes involved in cell division and DNA repair.
Importantly, the researchers found that removing SYCP1 made cancer cells much more sensitive to chemotherapy drugs that damage DNA. This suggests that cancers may exploit SYCP1 to repair treatment-induced DNA damage and continue growing.
Dr Urszula McClurg, Lecturer in Biochemistry, Cell and Systems Biology at the University of Liverpool said: "Our findings show that cancer cells can hijack proteins that normally exist only in reproductive tissues and give them completely new jobs. Understanding these unexpected functions opens up exciting opportunities to develop new treatments that make existing cancer therapies more effective."
The work also challenges the long-held view that proteins active only for fertility are biologically irrelevant outside the reproductive system. Instead, the study suggests that these specialised proteins may represent an untapped source of new therapeutic targets across many cancer types.
The research provides a new perspective on how cancers evolve by repurposing developmental and reproductive programmes, and highlights SYCP1 as a promising candidate for future precision cancer therapies.
The paper, 'Moonlighting role of meiotic SYCP1 in breast cancer: A chromatin-bound regulator of DNA repair, transcription, and drug resistance' was published in Science Advances (DOI: 10.1126/sciadv.aea2067)
