Published on 28th November 2018


Scientists at Hokkaido University in Japan have discovered how obesity impacts a natural mechanism that usually protects against cancers. 

Although a known risk factor for cancers of the colon, pancreas and breast, the role of obesity in triggering these diseases has been uncertain. 

Epithelial cells, which line the surfaces of organs, are normally able to get rid of potentially malignant cells; pushing them out in a process called ‘cell competition’. To study how obesity might affect this defence mechanism, the team bred mice designed to express a known cancer-inducing mutant protein called ‘Ras’. Normally, the epithelial cells will remove potentially malignant Ras-transformed cells. 

But feeding high-fat diets to the Ras mice, which resulted in severe obesity, suppressed this defence mechanism and increased the number of Ras-transformed cells remaining in the tissue. This suppression was seen in the intestine and pancreas, but not in the lungs. Furthermore, a month later, the Ras-transformed cells developed a tumour in the pancreas of mice with the high-fat diet. Follow-up experiments using the mice model and cultured cells also revealed that fatty acids and chronic inflammation caused the suppression of the defence mechanism. 

However, when the high-fat diet mice were treated with aspirin, which has anti-inflammatory properties, the defence mechanism was substantially enhanced. The authors concluded that this implied that reinforcing the epithelial defence mechanism with anti-inflammatory drugs could be used in cancer prevention. 

“This is the first report to show that obesity and chronic inflammation can influence competitive interaction between normal cells and transformed cells. It implies other factors such as infection, smoking, sleeping patterns and ageing may also affect cell competition,” said lead researcher Professor Yasuyuki Fujita of Hokkaido University. 


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