CD36 Accelerates Cancer Metastasis
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For the first time, researchers at the Institute for Research in Barcelona (IRB) have found the protein CD36 on cancerous cells which have the tendency to spread. The study was partially supported by UK charity Worldwide Cancer Research and led by Professor Salvador Aznar Benitah at IRB. CD36, seen in membranes of the cancer cells, is playing a major role in fatty acids intake. This distinctive activity of CD36 and fatty acid dependence differentiate cells which initiate metastasis from other cancerous cells.
Cancer is extremely life threatening when it spreads to other parts of the study; at this stage therapy is very complicated. Scientists are now trying to identify how cancer spread happens so they can discover new methods to block it.
Researchers noticed that CD36 is present on metastatic cancer cells from patients with various tumours such as melanoma lung, breast, ovarian, bladder, skin cancer and oral tumours. To affirm the tendency of CD36 in spreading cancer, they included it to non-metastatic tumor cells which then transformed into metastatic cells.
Even though we have not tested this in all types of cancer, we can say that CD36 is a common marker of metastatic cells, the primary thing I know about that is normally peculiar to metastasis, explains Professor Benitah, who serves as the Head of the IRB's Stem Cell and Cancer Lab.
We anticipate this study may lead to advancements in metastasis studies. We hope that we can evaluate the CD36's potential as an anti-metastasis therapy.
The researchers then observed the role of fat intake on cancer metastasis. They fed mice with high fat food and then injected them with human oral cancer cells. The high-fat food led to frequent and larger metastasis on 50 percent of the mice.
They continued to test a particular fatty acid known as palmitic acid, a key component of animal and vegetable fats which is abundantly present in palm oil and is used in several household items like toothpaste and processed food. The researchers administered palmitic acid on human oral tumor cells for two days then injected them into mice which were provided a normal diet. The research team found that every mice with CD36 had cancer metastatsis compared to those without palmitic acid.
In mice infected with human oral cancer cells, there exists a direct connection between fat intake and a rise in metastatic potential because of CD36. Further studies are required to disintegrate this relationship, especially since developed countries are showing a substantial raise in the intake of sugar and saturated fats, mentions Professor Benitah. “Fat is essential in the functions of the body, but excess intake may have a bad effect on health, as previously revealed in some cancers such as colon cancer, and in metastasis, as we show here.”
By observing mice with oral cancer, the researchers were then able to demonstrate that stopping CD36 entirely prohibited metastasis. In mice with tumour cells that have previously metastasized, CD36 antibodies resulted in the entire removal of metastases in 20% of the mice, while in others, it resulted to a remarkable decline of 80-90% in terms of metastases and a decrease in size. Prominently, these were all accomplished with no severe side effects.
The researchers are now creating new antibody-based treatments against CD36 that might potentially treat many types of cancers in the days to come.