Luke Noon, an expert at the Prince Philip Research Center (CIPF) and the Center for Biomedical Research in Network for Diabetes and Associated Metabolic Diseases (CIBERDEM), together with a team of scientists from Mount Sinai Hospital in New York, has discovered a new path that links metabolic syndrome and liver cancer.
This study, published recently in Nature Communications, demonstrates that the process of recycling cellular components active in healthy cells (known as autophagy) prevents the accumulation of a protein involved in tumor growth.
The effects detected by blocking autophagy in the livers of mice were very similar to those seen in human patients with non-alcoholic fatty liver disease (NAFLD), a chronic disease that increases the risk of developing liver cancer.
These effects recorded are caused by the accumulation of Yes-associated protein (Yap) which, as this work shows, promotes changes in the behavior of liver cells, increasing the risk of cancer.
Reducing the progression of the disease
The researchers hope that this newly identified route will open new modes of intervention to reduce the progression of the disease and the development of cancer in patients with NAFLD. The project’s principal researcher, Youngmin Lee, of Mount Sinai Hospital, said: “our data provide new knowledge about a disease that affects approximately 10% of the population in the United States and one in 20 adults in Spain.”
These results associate the alterations of the metabolism and the activation of the Yap protein with the liver cancer. Metabolic syndrome is an important risk factor in chronic liver diseases and cancer.
Noon, part of the CIPF Molecular Neuroendocrinology Laboratory (led by Deborah Burks), added: “these studies provide new antitumorigenic strategies.”