A molecule that regulates cholesterol metabolism in the liver could also have a role in the development of the most common type of liver cancer, according to US research.

Mice lacking the 'micro-RNA' molecule miR-122 in their liver cells develop fat deposits, inflammation and tumours that resemble a liver cancer called hepatocellular carcinoma (HCC), showed scientists from Ohio State University Comprehensive Cancer Centre.

The researchers say that restoring the molecule might slow tumour growth and offer clues into new ways to treat the disease in some liver cancer patients.

Dr Michaela Frye, a Cancer Research UK scientist at the University of Cambridge, said: "This is an important and solid piece of research that highlights our growing understanding of micro-RNAs in cancer development. The researchers have convincingly demonstrated that the loss of miR-122 in the liver induces liver inflammation, and that this can lead to liver cancer."

When the scientists artificially restored miR-122 to nearly normal levels by delivering the miR-122 gene into liver cells, it dramatically reduced the size and number of tumours in the mice.

Lead researcher Dr Kalpana Ghoshal said: "These findings reveal that miR-122 has a critical tumour-suppressor role in the healthy liver, and they highlight the possible therapeutic value of miR-122 replacement for some patients with liver cancer."

More than 3,900 people in the UK are diagnosed with liver cancer every year. Although HCC can be successfully treated if caught early, people are often diagnosed when their disease is advanced and more aggressive.

MiR-122 helps regulate the body's cholesterol levels. People with lower levels of the molecule often have more aggressive disease that is more likely to spread.

Long-term infection with hepatitis B or C increases the risk of developing liver cancer because it causes damage to the liver called cirrhosis.

Dr Ghoshal says her team's research might also contribute to a safer understanding of drugs to fight hepatitis C, as previous research has shown that the virus requires miR-122 to replicate.

The research is published in the Journal of Clinical Investigation.

Source: CRUK