Scientists identify new way to 'kill' cancer cells

New insight into how cells self-destruct could inform treatment approaches

Researchers have discovered a key process involved in cell death, which also stops cancer from spreading. PA

Scientists have identified a pivotal process in cellular self-destruction, known as apoptosis, which may play a significant role in inhibiting the spread of cancer.

The team of researchers shed light on the early stages of the process in which cells considered no longer necessary activate a “death programme”, resulting in self-destruction.

These findings could offer valuable insights on halting the proliferation of cancer cells, paving the way for potential new treatments, according to the report published in the scientific journal Science Advances.

The principal investigator, Luke Clifton of the Science and Technology Facilities Council’s ISIS Neutron and Muon Source in Oxfordshire, shared his optimism about the implications of the discovery.

“This work has both advanced our knowledge of fundamental mammalian cell processes and opened exciting possibilities for future research,” he said.

“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.”

The significance of apoptosis is vast. It is essential for human life, affecting numerous biological processes, including immune system regulation.

Crucially, it aids in the removal of harmful or potentially cancerous cells from the body.

Two proteins, Bax and Bcl-2, control apoptosis in healthy cells.

Researchers have identified the molecular mechanism of the early stages of programmed cell death, or apoptosis. PA

Bax protein, in particular, plays a vital role in removing old or diseased cells. Upon activation, it forms small holes, known as pores, in the cell's mitochondria membrane, initiating apoptosis.

Bcl-2, conversely, embedded within the same membrane, can inhibit premature cell death by capturing Bax proteins.

In cancerous cells, an overproduction of Bcl-2 can result in unchecked cell growth.

Unlike normal cells, which cease growing and dividing when enough exist, cancer cells may continue to proliferate, leading to tumour growth.

In a novel discovery, the scientists noted that Bax, in the act of pore creation, extracts lipids, or fatty compounds, to form clusters on the mitochondrial surface.

This research marks the first time scientists have established direct evidence of mitochondrial lipids' role in the apoptosis process.

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

“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 study also suggests that by leveraging Bax protein to initiate cell death, new avenues for cancer treatment could emerge.

Gerhard Grobner of Umea University in Sweden and study co-lead shared his enthusiasm for the groundbreaking findings: “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.”