High-Fat Diet Increases Cancer Metastasis in Mice

The list of different lifestyle factors that could cause cancer seemingly grows by the day. Recently, that list grew longer, as new groundbreaking evidence revealed that a high-fat diet may increase the spread of cancer.

Investigators discovered that CD36 was present on metastatic cancer cells. This discovery was observed on a range of tumors, including oral tumors, in addition to melanoma, skin, ovarian, bladder, lung, and breast cancers.

In a study published in Nature, the study authors set out to confirm its essential role in cancer metastasis by adding CD36 to non-metastatic cancer cells. They found that by adding CD36, it causes the cells to become metastatic.

“Although we have not yet tested this in all tumor types, we can state that CD36 is a general marker of metastatic cells, the first I know of that is generally specific to metastasis,” said investigator Salvador Aznar Benitah. “We expect this study to have a big impact on the scientific community and to further advances in metastasis research, and we hope to be able to validate the potential of CD36 as an anti-metastasis treatment. Things like this don’t happen every day.”

For the next step of the study, the investigators looked at the role fat intake has on cancer spread. Mice were given a high-fat diet, and were injected with a type of human oral cancer. The results of the study showed that the high-fat diet caused 50% more mice to have larger and more frequent metastases.

A specific fatty acid, called palmitic acid, was also tested. This acid is a major component of animal and vegetable fats, and present high-levels in palm oil. The human oral tumors were treated with palmitic acid for 2 days, then injected in mice given a standard diet.

The results of the study showed that all of the mice with CD36 developed metastasis compared with only one-half when not treated with palmitic acid.

“In mice inoculated with human tumor cells, there appears to be a direct link between fat intake and an increase in metastatic potential through CD36,” Benitah said. “More studies are needed to unravel this intriguing relationship, above all because industrialized countries are registering an alarming increase in the consumption of saturated fats and sugar. Fat is necessary for the function of the body, but uncontrolled intake can have an effect on health, as already shown for some tumors such as colon cancer, and in metastasis, as we demonstrate here.”

The study demonstrated that blocking CD36 completely prevented metastasis in mice with human oral cancer. In mice with cancer cells that had already spread, CD36-blocking antibodies led to the complete removal of metastases in 20% of the mice. In other mice, it caused a dramatic reduction of 80% to 90% of metastases and reduced the size without any serious adverse events, according to the study.

The investigators are currently developing new antibody-based therapies against CD36 that could potentially treat an array of cancer patients in the future.

“We have been supporting Professor Benitah’s work for a number of years and it is fantastic to now see these truly game-changing results,” said Dr Lara Bennett, science communication manager at Worldwide Cancer Research. “If the team are able to go on to develop this antibody into a treatment for humans it could save thousands of lives every year.”