Fat intake may fuel cancer’s ability to spread
We now have more evidence that fat fuels cancer’s spread
Scientists have stopped metastasis in mice.
Metastasis is the leading cause of cancer-related deaths in the world, but until now, scientists have struggled to understand exactly how and why cancer cells go through the energy-intensive process of splitting off, travelling through the bloodstream, and taking root somewhere else in the body.
In the past, it was assumed that sugar was cancer’s main fuel source, but a study earlier this year suggested that we’d been looking at metastasis entirely wrong – what if fat was actually driving the spread of cancer?
Now a team of researchers has shown that by blocking these cells from absorbing fat they can actually stop cancer from metastasising in mice – and they’re hoping the results might help them do the same in humans.
A team of researchers identified the cells responsible for the spread of oral cancer in mice, and showed that they rely on fatty acids – including palmitic acid, a major component of common food additive palm oil – to spread around the body.
They figured this out after noticing that many of the metastasising cells expressed high levels of a receptor protein called CD36, which helps cells absorb lipids.
High expression of CD36 has also been linked to poor medical outcomes in cancer patients, so the team decided to see what would happen if the receptor was blocked. Incredibly, the researchers showed that when they blocked CD36 expression in a range of human cancer cells, they were able to stop the cancer from spreading altogether in mice – although it didn’t stop primary tumours from forming. In mice, blocking CD36 with antibodies eradicated metastatic tumours 15 percent of the time, and the remaining tumours that had spread shrunk by at least 80 percent.
“We hypothesise that metastatic cells rely so much on the availability of certain fatty acids, that they cannot cope without them,” lead researcher Salvador Aznar Benitah commented.
“However, we still do not know the precise mechanism of why blocking CD36 results in such a strong effect on metastasis.”
While the team still has more work to do, their results so far show that the approach might also work after cancer has metastasised.
The research has been published in Nature.