The unhealthy effects of higher cholesterol – specifically LDL, the “bad” type – are recognized contain cardiovascular disease, stroke and atherosclerosis. But in a new research, scientists have identified how cholesterol triggers a cellular signaling pathway connected to cancer. The scientists, lead by Prof. Wonhwa Cho, presented their results in Nature Communications.
Earlier studies have linked cholesterol to specific cancers. For instance, Clinical Research Society recently reported on a research that high cholesterol leads to enhanced breast cancer possibility.
But for this most recent study, the scientists concentrated on signaling pathways, which cells implement to perform their regular activities. They describe that a process known as canonical Wnt signaling motivates cell development and division, an essential function for growth in embryonic cells.
However, in mature cells, over-activity of this process is considered to be a significant promoter of cancer progression.
When Prof. Cho and his group were looking for new cholesterol binding proteins, they identified a binding site for cholesterol placed on a protein well-known as “Dishevelled.” This protein is engaged in both canonical Wnt signaling and non-canonical Wnt signaling, which the group claims is engaged in cell movement and organization.
“Our study points to a new regulatory role for cholesterol,” states Prof. Cho, “and also provides an interesting new therapeutic
target for controlling canonical Wnt signaling to cure or protect against cancer.”
Cholesterol encourages signal to be sent along canonical Wnt pathway
The group additionally explains Dishevelled as ” activate the track,” which means that when a signal reaches the protein, it guides the signal along either the canonical or the non-canonical Wnt path.
However, till now, it was unidentified as to whether any specific element governed the choice for the protein to direct the signal down one pathway over the other.
This is where cholesterol comes into play, describes Prof. Cho:
“Once we noticed that cholesterol is capable to bind particularly to Dishevelled, we became fascinated in cholesterol as a possible determinant of which of the Wnt signaling pathways becomes activated.”
In depth, he and his team identified that when cholesterol binds to Dishevelled, it delivers the signal along the canonical Wnt signaling pathway – which promotes cell development and division. Without cholesterol, this kind of signaling can’t takes place, they add.
In addition, the scientists identified that cholesterol boosts within the cell membrane appeared to benefit canonical Wnt signaling over non-canonical Wnt signaling. Prof. Cho states that this may describe why higher cholesterol levels enhance cancer possibility.
The team says their results could provide a therapeutic target, and Prof. Cho states that a drug that stops cholesterol from joining to Dishevelled could be successful towards canonical Wnt signaling pushed cancers. This could consist of colon cancer, breast cancer , lung cancer and melanoma cancer.
“We know that things like high fat diets, which increase cholesterol levels, have been connected to an raised incidence of cancer,” he says. “Our study offers a mechanism for how cholesterol stimulates pathways that cause cancer.”