LONDON, Sept. 23 (Xinhua) -- Researchers have identified a mechanism that allows some aggressive cancers to survive when deprived of their normal energy supply, a finding that could offer a new way to slow tumor growth and improve the effectiveness of existing treatments, the University of Sheffield said on Wednesday.
The study, led by researchers at the university and published in the journal PLOS Biology, focused on aggressive breast and pancreatic cancers surrounded by dense, scar-like tissue known as the extracellular matrix.
According to the university, the extracellular matrix can account for up to 90 percent of the mass of some breast and pancreatic tumors. While the dense tissue restricts blood supply and the delivery of nutrients, cancer cells can adapt by using type I collagen, a major component of the matrix, to help them survive.
The researchers found that when levels of glucose, normally a major energy source for cells, fall, collagen activates signals that enable cancer cells to switch their source of fuel and take up essential amino acids needed for growth and survival.
The process depends on a transporter protein known as LAT1, which helps move amino acids into cancer cells. Laboratory experiments using cellular models showed that blocking LAT1 while disrupting the interaction between cancer cells and collagen deprived the cells of vital nutrients, according to the university.
Dr. Elena Rainero, senior lecturer at the University of Sheffield and lead author of the study, said cancer cells can adapt rapidly, which means a single treatment often fails to eliminate a tumor completely.
"If we can block this collagen-driven survival mechanism, we could slow the growth and spread of cancer cells while making them more sensitive to existing treatments like chemotherapy," Rainero said.
She said such an approach could potentially allow clinicians to use lower treatment doses, reducing severe side effects while improving treatment effectiveness.
The researchers said the findings could offer a promising target for future cancer therapies. ■