Research links protein to breast-cancer migration

The University of Manchester team has discovered a protein potentially involved in the spread or ‘metastatic progression’ of tumours.

The researchers believe their findings could lead to new approaches to treating breast cancer as blocking the protein’s actions has the potential to stop cancerous cells migrating.

“What we have identified is a new role for a protein called LPP,” explained Professor Andrew Sharrocks, who headed the research team.

“Until now, this protein was only thought to function at the cell periphery but we have shown that it works in conjunction with another protein – PEA3 – in the cell nucleus.

“PEA3 has already been implicated in the spread of breast cancer but we have found that the LPP molecule is essential for the correct function of PEA3.”

“If we can target the LPP protein and stop it from working in cancerous cells, we have a possible new route to therapy.”

The research, published in the scientific journal Molecular and Cellular Biology, may have implications for other cancer systems.

“Benign tumours remain in one part of the body and are relatively easy to treat through surgery,” said Professor Sharrocks, who is based in the University’s Faculty of Life Sciences.

“But metastases – malignant cancers that spread to other parts of the body – can be much more problematic.

“Our research is potentially fundamental to all types of cancers and has the potential to offer alternative therapies to stop cancers spreading to other organs in the body.”

News of the scientific breakthrough comes as the University announced Breast Cancer Campaign funding for two other research projects worth nearly £300,000.

Dr Andrew Gilmore, also in the Faculty of Life Sciences, has been awarded a grant of £146,000 to examine in more detail a process called ‘anoikis’.

Anoikis is the process whereby the body ambushes and kills roving cells that have gone ‘AWOL’ and are moving around the body without permission – like breast-cancer cells that spread from the breast to form tumours in other parts of the body.

Current breast-cancer treatments have been designed to kick start the anoikis process and kill these rogue cells. But the cancer cells are clever and learn how to avoid being destroyed, which means these treatments no longer work and patients often see their breast cancer return.

Dr Gilmore said: “Understanding more about how the body’s natural defences work and why breast-cancer cells can avoid them will help develop new drugs that can kill invasive cells that have become resistant to standard treatment.”

A further £143,000 has been awarded by the charity to Dr Keith Brennan, again in Life Sciences, to uncover how a group of proteins called Notch are able to protect breast-cancer cells from dying.

“Notch proteins appear to shield breast-cancer cells from the body’s natural defences and also from being destroyed by chemotherapy,” said Dr Brennan.

“This research will help to uncover exactly how Notch proteins have this effect and whether inhibiting their action may be one way of making chemotherapy treatments more effective.”

Pamela Goldberg, Chief Executive of Breast Cancer Campaign, added: “The spread of breast-cancer cells to other areas of the body is the single most important factor in breast-cancer mortality.

“When breast-cancer cells become invasive they become less responsive to treatment and the disease becomes more difficult for a clinician to manage.

“Both these studies could help to develop new drugs which kill breast-cancer cells before they have an opportunity to spread.”

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Aeron Haworth alfa

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