PULLMAN, Wash. — A universally effective and dependable way to treat cancer is seemingly harder to find than Atlantis or El Dorado. Hope abounds, though. Now, new research by Washington State University offers up the latest potential breakthrough in cancer treatments: a fatty acid.
The study’s authors demonstrate that the fatty acid known as dihomogamma-linolenic acid (DGLA) kills human cancer cells upon exposure.
More specifically, DGLA causes ferroptosis after coming into contact with cancer cells, as observed in both animals models and human cells. Ferroptosis is a type of cell death associated with iron dependence. Ferroptosis was only recently discovered, but since then it’s garnered lots of attention from disease researchers.
These findings are, of course, preliminary. Still, researchers believe their discovery could lead to a new form of cancer treatment in the future.
“If you could deliver DGLA precisely to a cancer cell, it could promote ferroptosis and lead to tumor cell death,” says corresponding study author Jennifer Watts, a Washington State University associate professor, in a release. “Also, just knowing that this fat promotes ferroptosis might also affect how we think about conditions such as kidney disease and neurodegeneration where we want to prevent this type of cell death.”
DGLA largely unstudied
Belonging to the polyunsaturated fatty acid family, DGLA can be found within the human body in small amounts. On rare occasions, it’s also in the food we eat. For the most part, however, DGLA is somewhat of mystery in modern medicine as research on it remains quite thin.
This isn’t professor Watts’ first fatty acid rodeo; she’s been studying various dietary fats for over 20 years. Most of the time, her research is facilitated by a microscopic worm known as C. elegans. It sounds somewhat odd at first, but this tiny worm is a frequent participant in molecular research because of its transparent appearance and short lifespan. Moreover, findings using C.elegans cells are typically applicable to human cells as well.
This time around, Watts says that feeding these worms a heavy diet of DGLA-housing bacteria results in all of the germ cells within the worms dying. Also, the DGLA even killed the worms’ stem cells, which produce germ cells in the first place. According to the study, the observed way in which the worms’ cells died suggested ferroptosis.
“Many of the mechanisms we saw in the nematodes were consistent with the hallmarks of ferroptosis in mammalian systems, including the presence of redox-active iron and the inability to repair oxidized lipids, which are like molecular executioners,” adds Marcos Perez, a WSU doctoral student and first author on the paper.
Cancer cells have a fatty acid shield?
Next, to see if the same results would occur in human cells, the team at WSU collaborated with Scott Dixon from Stanford University. Dixon has been studying the potential cancer-fighting benefits of ferroptosis for years.
Subsequent experiments with human cells indeed show that DGLA can jumpstart ferroptosis in human cancer cells. Furthermore, there’s also a noteworthy observation regarding another kind of fatty acid class. These fatty acids, known as ether lipids, display a protective tendency against DGLA. When these lipids are removed from human cancer cells, they die at a faster pace after being exposed to DGLA.
The study is published in Developmental Cell.