Protein linked to cell death may also drive liver cancer
New research from the University of Oklahoma identifies a protein in liver cells that appears to help drive the development of liver cancer associated with obesity-related fatty liver disease. The finding, published in Hepatology, points to the protein as a potential new therapeutic target for liver cancer.
Researchers at the University of Oklahoma have discovered that a protein called MLKL, known for its role in cell death, may also contribute to the development of liver cancer linked to obesity. Published in the journal Hepatology, the study found that MLKL levels increased in mice fed a high-fat diet. Instead of causing liver cell death, increased MLKL appeared to impair mitochondrial function and promote tumor growth.
When MLKL was removed from the mice, fewer and smaller liver tumors developed, providing a new potential therapeutic target for hepatocellular carcinoma, the most common type of liver cancer. The finding challenges the traditional view of liver cancer as a progressive disease, suggesting MLKL regulates tumor development through a different pathway.
The research team also found that higher MLKL levels in human liver cancer samples were associated with poorer survival rates. Further studies are planned to investigate MLKL as a potential drug target and a biomarker for liver cancer, as obesity-related fatty liver disease is becoming a significant contributor to liver cancer cases.
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