The discovery suggests that blocking the protein, known as SYCP1, could make cancer cells more sensitive to treatment and potentially provide a new target for future therapies.

The study, involving researchers from the Institute of Medical Biology of the Polish Academy of Sciences in Łódź and collaborators in France, Portugal, Spain and the United Kingdom, was published in Science Advances.

One of the biggest challenges in cancer treatment is distinguishing tumour cells from healthy cells. Cancer develops from the patient's own cells after they undergo dangerous genetic changes, rather than being a foreign organism.

As a result, many chemotherapy drugs damage healthy cells as well as tumours, particularly rapidly dividing cells in the bone marrow, hair follicles and gastrointestinal tract. This can cause side effects including hair loss, nausea and suppression of the immune system.

Scientists have therefore spent years searching for features that are more specific to cancer cells and could provide targets for more effective and less toxic treatments.

SYCP1 may be one such vulnerability.

The protein, whose full name is synaptonemal complex protein 1, is a key component of the synaptonemal complex, a structure involved in meiosis — the specialised cell division process that produces sperm and egg cells.

The complex brings corresponding chromosomes together, allowing them to exchange genetic material and then separate correctly into developing reproductive cells.

Defects in the gene encoding SYCP1 can cause fertility problems, including azoospermia, the absence of sperm in semen.

SYCP1 has also been known as a cancer-testis antigen. These are proteins normally produced mainly during the development of reproductive cells but whose genes can become abnormally reactivated in cancer.

Until now, however, its role in tumour cells was unclear.

An international team led by Urszula McClurg, PhD, of the Cell Cycle Laboratory at the Institute of Medical Biology of the Polish Academy of Sciences in Łódź, found that SYCP1 enters the nucleus of breast cancer cells and binds to DNA.

It then influences genes involved in cell division and the repair of damaged genetic material, allowing the cancer cells to continue multiplying.

This could be particularly important during chemotherapy because some anticancer drugs work by damaging tumour DNA. If cancer cells can efficiently repair that damage, they can avoid dying and survive treatment.

“Cancers can exploit mechanisms that are normally only active during the development of reproductive cells. By exploring these processes, we are uncovering new tumour vulnerabilities that may become targets for more precise and effective therapies in the future”, McClurg emphasises.

The researchers tested the role of SYCP1 by disabling the gene in laboratory-grown breast cancer cells.

The cells became less able to repair DNA, proliferated more slowly and had a reduced ability to migrate. They were also more sensitive to cisplatin and gemcitabine, drugs that damage genetic material.

The findings indicate that SYCP1 helps tumour cells maintain their ability to divide, migrate and survive treatment.

The researchers then performed the opposite experiment, activating SYCP1 in non-cancerous breast epithelial cells that normally do not produce the protein.

Those cells began multiplying faster and migrating more efficiently, suggesting that SYCP1 can give cells some cancer-promoting characteristics. However, the researchers found that the presence of the protein alone was not sufficient to cause cancer.

The team also analysed tumour samples from 137 breast cancer patients.

They found that high levels of SYCP1 were associated with shorter overall survival. The researchers stressed, however, that this association does not prove that the protein directly causes poorer outcomes.

The finding nevertheless suggests that SYCP1 could potentially be developed as a biomarker to help assess the course of the disease.

The results also point to SYCP1 as a possible target for future cancer treatments. Inhibiting the protein could make tumour cells more vulnerable to DNA-damaging chemotherapy and potentially reduce the need for high doses of toxic drugs.

McClurg emphasises that this discovery represents another step in understanding how cancers reprogram their own cells to survive treatment and continue to grow. It also demonstrates that proteins previously considered important only for fertility may play a key role in cancer development, paving the way for the development of a new generation of precision cancer therapies.

The study was conducted by researchers from Poland, France, Portugal, Spain and the United Kingdom.

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The EMBO cancer research conference was held in Łódź from July 27 to 29, bringing together researchers focusing on cancer biology and new approaches to treatment. The conference was part of the EMBO events programme and was organised for scientists who are members of the EMBO Young Investigator Network.

Katarzyna Czechowicz (PAP)

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