Scientists have discovered a key process that is involved when the body’s cells die, which also stops cancer from spreading.

Researchers have identified the molecular mechanism of the early stages of programmed cell death, or apoptosis, where cells that are no longer needed undergo self-destruction by activating the co-called “death programme”.

They said the findings, published in the journal Science Advances, could potentially provide insight on how to stop cancer cells from multiplying and open doors to new treatments.

Understanding what things look like when cells work properly is an important step to understanding what goes wrong in cancerous cells

Dr Luke Clifton, of the Science and Technology Facilities Council’s ISIS Neutron and Muon Source in Oxfordshire, who led the research, said: “This work has both advanced our knowledge of fundamental mammalian cell processes and opened exciting possibilities for future research.

“Understanding what things look like when cells work properly is an important step to understanding what goes wrong in cancerous cells and so this could open doors to possible treatments.”

Apoptosis is crucial for human life and plays a significant role in various biological processes such as immune system regulation.

It also helps eliminate potentially harmful or cancerous cells from the body.

In healthy cells, apoptosis is regulated by two proteins, Bax and Bcl-2.

The Bax protein is responsible clearing old or diseased cells from the body.

When activated, it makes tiny holes – pores – in the membrane of the cell’s mitochondria – small, energy-producing structures found within cells – to trigger apoptosis.

But in some cases, this can be offset by Bcl-2, which is embedded within the mitochondrial membrane, where it acts to prevent untimely cell death by capturing and sequestering Bax proteins.

However in cancerous cells, Bcl-2 is overproduced, which, in turn, can lead to uninhibited cell growth.

Normal cells stop growing and dividing when there are enough of them, but cancer cells can keep on proliferating, forming a tumour that grows in size.

The scientists found that when Bax creates pores in the membrane, it extracts lipids (fatty compounds) to form clusters on the mitochondrial surface.

According to the researchers, this is the first time that scientists have found direct evidence of the involvement of mitochondrial lipids in the cell-death process.

Dr Clifton said: “As far as we can tell, the mechanism by which Bax initiates cell death is previously unseen.

“Once we know more about the interplay between Bax and Bcl-2 and how it relates to this mechanism, we’ll have a more complete picture of a process that is fundamental to human life.”

The team said that harnessing the power of the Bax protein to trigger cancer cell death could open the doors to new types of cancer treatments.

Professor Gerhard Grobner, of Umea University in Sweden, and study col-lead, said: “The unique findings here will not only have a significant impact in the field of apoptosis research but will also open gateways for exploring Bax and its relatives as interesting targets in cancer therapy such as by tuning up their cell-killing potential.”