Survival rates for eye cancer are generally high, according to the American Cancer Society.
However, when it becomes metastatic — that is, when cancer cells break away and travel elsewhere in the body to form more tumors — this rate can drop significantly.
Finding a way to slow down the progression of eye cancer is therefore crucial.
Researchers in Germany believe that they might have found such a method, and it is all thanks to one plant.
The coralberry originates in Korea. Its bright red fruit makes it an ideal decoration, especially during the holiday season. Due to this popularity, scientists have examined its parts in great detail.
Its leaves contain bacteria that result in a form of natural insecticide called FR900359 (FR). This has been on the science community’s radar for 30 years.
The substance protects the coralberry from insects and has been the focus of a study that claimed that FR could treat asthma more effectively than standard medication.
FR is also the subject of a new study, the results of which appear in the journal Science Signaling.
Alongside colleagues in the United States, researchers from the Universities of Magdeburg and Bonn, both in Germany, believe that they have found a new use for the toxin.
Coralberry’s surprising impact
“The substance inhibits an important group of molecules in the cells, the Gq proteins,” explains Dr. Evi Kostenis, from the University of Bonn’s Institute of Pharmaceutical Biology.
These proteins act similar to an emergency control center. When a signal activates them, they can turn cells’ metabolic pathways on and off. However, this only happens for a short period of time, after which the cell returns to its normal state.
In a particular form of eye cancer called uveal melanoma, two Gq proteins remain permanently active. The mutation that causes this results in cells dividing continuously.
Cancer’s cause is currently unknown, but it is more common in people who have fair skin and blue or green eyes.
Just five to six cases per million people occur each year, according to the University of Michigan Kellogg Eye Center in Ann Arbor. This increases to around 21 cases per million people in those over the age of 50.
Scientists already know that FR can stop Gq proteins from being activated by clinging onto them. However, what researchers have now found is that FR can halt cell division. “That’s something no one would have expected,” says Dr. Kostenis.
This was surprising because scientists believed that FR would disregard activated Gq proteins. It, therefore “seemed impossible” that the substance could work in mutated proteins, explains Dr. Evelyn Gaffal, now at the University of Magdeburg.
Diving deeper into the mechanism
As well as showing that FR is effective on both active and inactive proteins, their study also reveals how this happens. The team found that mutated, permanently active Gq proteins sometimes return to their inactive state.
At this moment, FR holds onto the protein in the same way as before, preventing it from activation. As time goes on, more and more Gq proteins are returned to inactivity, potentially slowing down uveal melanoma.
Scientists have seen this effect in cell cultures and in the cells of mice with cancer. However, there is some way to go before they can test it in humans.
Ensuring that FR targets only tumor cells — not other tissues — will be the next step. However, as Dr. Kostenis notes, “this is a challenge that many other chemotherapies also have to deal with.”