
Cancer cells may hijack a fertility protein to repair damaged DNA and survive chemotherapy, research suggests.
The findings could point to a way of making existing cancer treatments more effective.
SYCP1 is a protein normally involved in producing sperm and eggs.
Researchers at the University of Liverpool found that the protein, previously thought to work only in reproduction, can be reactivated in cancer cells, where it helps tumours survive and grow.
SYCP1 usually helps chromosomes pair during meiosis, the form of cell division that produces reproductive cells.
In cancer cells, however, the protein appears to take on another role. It enters the nucleus, the cell’s control centre, binds directly to DNA and regulates genes involved in cell division and DNA repair.
DNA repair is how cells fix damage to their genetic code. In cancer, this process can help tumour cells survive treatment.
The researchers found that removing SYCP1 made cancer cells much more sensitive to chemotherapy drugs that damage DNA.
The findings suggest cancers may use SYCP1 to repair damage caused by treatment 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 challenges the long-held belief that proteins active only in fertility have no biological relevance outside the reproductive system.
Researchers say these specialised proteins could provide new treatment targets across many types of cancer.
The study also offers a new view of how cancers evolve by repurposing developmental and reproductive processes.
The findings highlight SYCP1 as a candidate for future precision cancer therapies, which are treatments based on the specific biology of a patient’s cancer.
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