Obesity has long been known as a major health risk. It has also been associated with the development of aggressive cancers. By studying underlying mechanisms related to the phenomena, researchers found that the presence of adipose tissue around the prostate gland of obese patients promotes the development of tumor cells outside the prostate.
Periprostatic adipose tissue (PPAT) is a fatty deposit that surrounds the prostate. As prostate cancer progresses, tumor cells invade the PPAT, signaling locally advanced disease. Obese patients don’t just have enlarged PPAT cells, but a greater number of them as well. Unfortunately, PPAT cells produce bioactive molecules, like chemokines, that attract other cells.
In a study published in the journal Nature Communications, researchers sought to investigate whether the spike in PPAT cells was the reason prostate cancer was more aggressive in obese patients. They found that a chemokine called CCL7 interacts with a receptor known as CCR3 on the surface of prostate cancer cells. The interaction facilitates the progression and spread of prostate cancer and obesity amplifies the mechanism.
While testing the influence of obesity on the CCL7-CCR3 interaction, the researchers found that obese mice fed high-fat diets had faster tumor progression and spread outside the prostate compared to mice with normal weight. When tumor cells no longer capable of expressing CCR3 were implanted on mice prostates, tumor progression and spread was reduced significantly, particularly in obese mice.
When the researchers observed the mechanism in men, they discovered that obese patients secreted higher levels of CCL7. After examining over 100 samples of human tumor, they also found that tumors with a lot of CCR3 present were also more likely to spread and be more resistant to treatment.
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