Omega-6 fatty acids cause prostate tumour cell growth in lab

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Related tags: Omega-6 fatty acids, Cancer

Omega-6 fatty acids promote the growth of prostate tumour cells in
the laboratory, according to US researchers, who say they have also
identified a mechanism for this action.

The scientists suggest that a rapid increase in the amount of omega-6 fatty acids in the western diet could have caused the rise in incidence of prostate cancer in recent years.

Their findings are not the first to connect this group of fatty acids to cancer. Omega-6 fats have also been linked to the development of breast cancer, with a Spanish team reporting last year that the fats enhanced expression of certain genes that accelerate the disease.

In the new study, Dr Millie Hughes-Fulford, director of the Laboratory of Cell Growth at the San Francisco VA Medical Center (SFVAMC) and colleagues introduced arachidonic acid, an omega-6, into human prostate tumour cells in culture. They found that they caused the production of the enzyme cPLA2.

This then caused the production of the enzyme COX2, which in turn stimulates the release of PGE2, a hormone-like molecule that promotes cell growth.

Hughes-Fulford says this is the first time a direct chain of causation has been demonstrated. Her findings will be published in the September 2005 issue of Carcinogenesis​, currently available online.

"What's important about this is that omega-6 fatty acids are found in corn oil and most of the oils used in bakery goods,"​ said Hughes-Fulford.

"Which means that if you're eating a diet high in omega-6 fatty acids, it's possible that you're turning on this cancer cascade, which has been shown to be a common denominator in the growth of prostate, colorectal, and some breast cancers."

Around 60 years ago, the dietary ratio of omega-6 to omega-3 in the US was one to two. Today, the ratio is 25 to one. Over that same 60 years, the incidence of prostate cancer in the US has increased steadily, say the study authors.

Hughes-Fulford also found that flurbiprofen, a non-steroidal anti-inflammatory drug commonly prescribed for arthritis, blocked the production of cPLA2 and broke the chain leading to cell growth, pointing to a new drug development target.

"COX2 has been implicated in the growth of many types of tumours,"​ noted Hughes-Fulford. "So if you can find a way to block that cascade in the tumour, starting with cPLA2, you might have a new way of modifying or slowing tumor growth."

Furthermore, cPLA2 inhibitors would avoid the problems inherent in the class of drugs known as COX2 inhibitors, until recently a common treatment for the pain associated with inflammatory conditions such as arthritis but now implicated in increased risk of cardiovascular problems among regular users.

Hughes-Fulford plans to investigate further the overall effect of different types of fatty acids on different tumour types in cell lines as well as human biopsies.

Her work will include a study that will correlate type of fatty acid with tumour stage and grade in order to obtain a clearer picture of specific effects of different fats on tumour progression.

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