Cancer Update: The role of 20-HETE metabolite in the spread of cancer

One of the tricky parts of treating cancer is the fact that it can metastasize to other parts of the body. Once the cancerous cells have spread, it becomes harder to treat. Thankfully, a recent breakthrough reveals that there may be a way to stop cancer from spreading.

How 20-HETE helps spread the cancer

Published in PLOS ONE,the study talked about how inhibiting the 20-HETE metabolite can stop the cancer from spreading elsewhere. In an article published in Medical News Today, 20-HETE or 20-Hydroxyeicosatetraenoic acid is  explained  as “a breakdown product of arachidonic acid, a fatty acid used widely throughout the body. 20-HETE carries out a number of useful roles, including the regulation of vascular tone, blood flow to organs, and sodium and fluid transport in the kidney. The metabolite also plays a role in inflammation, helping the body fight off infections and other diseases.”

This is where it gets interesting: when the body is compromised with cancerous cells, the tumors can hijack the function of 20-HETE, and the metabolite helps the cancer spread to other places. To explain this further, one has to understand how cancerous cells are spread into the body. First, the cancerous cells have to detach from their current position. They have to be strong enough to journey to the new location. Once there, they have to find supporting blood vessels and tissues to create an environment that would foster the growth of the tumors. 20-HETE, therefore, prepares the new location by encouraging the new cells to accept the cancerous cells, making them grow.

Since 20-HETE is instrumental in the spread of cancer, the researchers, therefore, explored how they can inhibit 20-HETE. They found that a molecule called HET0016 can do just that. The researchers injected the molecule into mice which have displayed signs that cancer has spread, and gave it to them for five times a week for three weeks.

To say that the results are astounding was an understatement. In just 48 hours, the ability of cancer cells to move freely was limited. Protein structures were also destroyed, enabling new blood vessels to grow. Other molecules that hasten the growth of cancer were also limited, such as myeloid-derived suppressor cells. Dr. Ali S. Arbab, the study lead, said, “It gets rid of one of the natural protections tumor use, and tumor growth in the lung goes down.”

While the study still needs refinement to be able to transition for human use, the authors believe that targeting 20-HETE can be beneficial in prohibiting cancer from growing. This is similar to the approach of some drugs in the market, which have hijacked the molecular pathway to prevent cancer from spreading.

The study continues to provide insight and hope for the medical community. After all, many cases of metastasized cancer have significantly diminished the patient’s chances of survival. If the potential of cancer is found — and in effect, enacted so that it cannot spread further — then the number of casualties from metastasized cancer would also be significantly reduced.