Cancer research: fatty acid destroys cancer cells

Cancer research: fatty acid destroys cancer cells

We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

How a fatty acid causes cancer cell death

A fatty acid called dihomogamma-linolenic acid (DGLA) is able to kill human cancer cells. An American research team showed that DGLA initiates ferroptosis in cancer cells. Ferroptose is an iron-dependent type of cell death that was only discovered a few years ago.

Washington State University researchers found that the fatty acid dihomogamma-linolenic acid (DGLA) can kill cancer cells by triggering a process called ferroptosis that destroys the membranes of the tumor cells. This could open up a whole new way of fighting cancer. The research results were recently presented in the "Developmental Cell" journal.

What is ferroptosis?

Ferroptose is an iron-dependent type of cell death that has been discovered in recent years and has become a new focus of cancer research. In this iron-dependent process, reactive oxygen species accumulate on the building blocks of cell membranes (membrane lipids). By enriching oxygen species in the presence of iron, the lipids eventually oxidize, destroying the membrane and killing the cell.

DGLA initiates ferroptosis

The Washington State University research team is now introducing a fatty acid that uses this process to kill cancer cells. "If you could insert DGLA exactly in a cancer cell, it could promote ferroptosis and lead to the death of tumor cells," reports the corresponding study author Professor Jennifer Watts. In addition, deciphering this process can also help with kidney diseases and neurodegeneration, where ferroptosis is to be prevented.

What is DGLA?

DGLA is a polyunsaturated fatty acid that only occurs in very small amounts in the human body. It is also very rarely found in human nutrition. In contrast to other fatty acids, DGLA has so far been little researched.

Will there be an anti cancer diet soon?

In experiments on the roundworm Caenorhabditis elegans, also called nematodes, the team showed that DGLA kills tumor cells and stem cells that produce tumor cells. The researchers enriched the worms' diet with the fatty acid, whereupon the tumor germ cells in the worms died.

"Many of the mechanisms that we saw in the nematodes were consistent with the characteristics of ferroptosis, including the presence of redox-active iron and the inability to repair oxidized lipids," added study author Marcos Perez.

Checked on human cells

To see if the results were transferable to human cells, the researchers consulted a team at Stanford University that has been testing ferroptosis as an option to fight cancer for many years. The scientists were able to show that DGLA can also induce ferroptosis in human cancer cells.

They also found an opponent: fats from the ether lipid class seem to prevent ferroptosis and protect the cell from this type of death. When the researchers inhibited these fats, the cells died faster with DGLA.

Great potential to fight cancer

The American National Institutes of Health showed great interest in the research results and added $ 1.4 million to the research budget to advance the studies in this area. DGLA and ferroptose have great potential to develop completely new cancer treatments. Before that, however, the underlying process needs to be better understood. (vb)

Author and source information

This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.

Graduate editor (FH) Volker Blasek


  • Washington State University: Study finds fatty acid that kills cancer cells (published: July 10th, 2020),
  • Marcos A. Perez, Leslie Magtanong, Scott J. Dixon, et al .: Dietary Lipids Induce Ferroptosis in Caenorhabditis elegans and Human Cancer; in: Developmental Cell, 2020,

Video: Keto and Cancer (February 2023).