KEY POINTS

  • Cancer is one of the leading causes of death worldwide
  • New study pointed out that a particular dietary lipid can induce cell death in cancer cells
  • Further research can pave the way towards an effective cancer treatment 

Dietary fats can affect cellular development, homeostasis, and disease. Dihomogamma-linolenic acid (DGLA), an extremely uncommon fatty acid present only in traces in animal products, can induce ferroptosis in a particular animal model as well in real human cancer cells, reported a new study.

Ferroptosis is an iron-dependent type of cell death that is associated with several disease progressions. This discovery about fatty acids can have several implications including a promising way to treat cancers.

“If you could deliver DGLA precisely to a cancer cell, it could promote ferroptosis and lead to tumor cell death. 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,” News Medical quoted Jennifer Watts, Associate Professor at Washington State University.

DGLA is a polyunsaturated fatty acid that is found rarely in the human diet and is relatively understudied compared to other fatty acids like those found in fish oil.

Watts and his team have been researching dietary fats including DGLA for almost two decades using the animal model nematode Caenorhabditis elegans (C. elegans).

The microscopic worm has been used in several molecular studies due to its transparent nature that allows scientists to easily study cell-level activity in a whole animal over its relatively short lifespan.

The researchers found that feeding these worms a diet of DGLA-laden bacteria destroyed all the germ cells in these nematodes alongside the stem cells that made them.

And to find out how these findings would translate to human cells, the research team collaborated with experts at Stanford University who has been analyzing the effects of ferroptosis in fighting cancer.

The researchers were able to demonstrate that DGLA could trigger cell death in human cancer cells. They also found interaction with an ether lipid which had a protective effect against DGLA. But upon removing these ether lipids, the cancer cells died faster in the presence of the fatty acid. The findings of the study also highlighted that C. elegans can be a useful animal research model.

“These results establish C. elegans as a powerful animal model to study the induction and modulation of ferroptosis by dietary fats and indicate that endogenous ether lipids act to prevent this nonapoptotic cell fate,” said the researchers in their paper published in Developmental Cell.