Washington, Sept 18: A new discovery linking cholesterol with cancer shows how cholesterol busting drugs, or statins, can prevent cancer or supplement its existing treatments.
The discovery was made by University of Rochester Medical Centre. It validates the theory that people with highest levels of cholesterol seem to have higher chances of cancer.
The cancer-cholesterol question has been debated since the early 20th century. However, until now, genetic evidence directly linking cholesterol and malignancy has been lacking, said senior study author Hartmut (Hucky) Land, professor and head of biomedical genetics at Rochester, the journal Cell reports.
"Scientifically it is very satisfying to have data that support longstanding ideas about cholesterol in the context of cancer," Land said. "Our paper provides a rationale for cholesterol targeting as a potentially fruitful approach to cancer intervention or prevention strategies."
Millions of people take statins, which work by blocking the action of key enzymes in the liver, which synthesizes cholesterol, according to a Rochester statement.
Cholesterol is a fat-like substance in foods and made in cells throughout the body. Too much cholesterol is bad for the heart and vascular system. It is typically measured as serum cholesterol by routine blood tests.
However, unlike serum cholesterol that is bound to proteins, cholesterol also hides inside cells. While locked inside cell membranes before it is eventually exported, cholesterol has an impact on cell growth and survival. A gene, known as ABCA1, is at the crossroads of the process that shuttles intracellular cholesterol outbound.
In the latest investigation, Land and co-author Bradley Smith, post-doctoral fellow in the Land lab, wanted to further understand the role of ABCA1 and cholesterol in cancer. They found that defective cholesterol exportation appears to be a key component in a variety of cancers.
Smith and Land also demonstrated that some of the relatively rare ABCA1 mutations found in human colon cancers by other investigators disabled the gene's ability to export cholesterol. And by re-establishing the cholesterol export function in human colon cancer cells, they inhibited the cells' ability to grow as cancers when grafted onto mice.
