Researchers at UT Southwestern Medical Center have found that eliminating the amino acid tryptophan from the diet can effectively stop the growth of liver cancer in mice.
This discovery, published in Nature Communications, suggests that dietary changes could be a powerful tool in cancer treatment.
The study also highlights the significant role of a tryptophan metabolite, indole 3-pyruvate (I3P), in the development of liver tumors.
The study was led by Dr. Maralice Conacci-Sorrell, Associate Professor of Cell Biology and Children’s Medical Center Research Institute at UT Southwestern (CRI), and a member of the Cellular Networks in Cancer Research Program at the Harold C. Simmons Comprehensive Cancer Center.
According to Dr. Conacci-Sorrell, “This work demonstrates that tailored dietary modulation may serve as a powerful adjuvant in cancer treatment.” The research builds on previous findings that the oncogene MYC increases the demand for tryptophan in liver tumors.
Liver cancer, specifically hepatocellular carcinoma (HCC), is the third-leading cause of cancer-related deaths worldwide, with a five-year survival rate of about 30%. The study shows that liver cancers driven by the MYC oncogene rely heavily on tryptophan, which is converted into I3P and other metabolites.
By removing tryptophan from the diet of mice, researchers were able to halt the growth of MYC-driven liver tumors and normalize gene expression in liver cells. Importantly, this dietary intervention did not affect protein synthesis in normal cells, suggesting that this approach could target cancer cells while sparing healthy tissues.
“Liver tumors require large amounts of tryptophan to generate the oncometabolite I3P,” explained Dr. Conacci-Sorrell. “A tryptophan-free diet prevents liver tumor growth by a mechanism that depends on I3P but is independent of translation, the process by which proteins are synthesized from amino acid building blocks.
Because tryptophan is the amino acid with the lowest abundance in the proteome, short-term dietary manipulation is safe for healthy tissues but not for cancer cells.”
Foods that are high in tryptophan include turkey, red meat, pork, chicken, tofu, milk, soybeans (including edamame), quinoa, oats, and fish.
The research also sheds light on the complex role of tryptophan metabolism in cancer. While tryptophan is usually metabolized into compounds like the neurotransmitter serotonin and kynurenine (a precursor of the B vitamin niacin), MYC-driven liver tumors prefer to use tryptophan to produce I3P.
This finding suggests that targeting specific metabolic pathways could be a viable strategy for cancer treatment.
Moreover, the study found that adding I3P back into the diet restored the growth of tryptophan-starved liver cancer cells, emphasizing the critical role of this metabolite in cancer development. This suggests that targeting I3P or its production pathway could be a promising therapeutic strategy.
“This study not only advances our understanding of liver cancer biology but also suggests a promising approach for developing personalized cancer therapies,” said Dr. Conacci-Sorrell.
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The research findings can be found in Nature Communications.
