03:58:56pm | 02-Feb-2019 | 980 | 79


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In a study on mouse models and human tissue, researchers have revealed how aggressive forms of skin cancer are able to co-opt the immune system to become invasive. Knowing this could lead to better, more effective treatments.

researcher looking at test tube

A study reveals the key factors that allow melanoma to become invasive.

New research, the findings of which now appear in the journal Cell, has found a mechanism that allows aggressive forms of skin cancer to become invasive and spread quickly.

The study, which nonprofit organization Cancer Research UK funded, was conducted by a team from King's College London and Queen Mary University of London (QMUL), both in the U.K.

In their experiment, they analyzed the makeup of skin cancer, or melanoma, cells, looking for the factors that work to their advantage.

They found that such cancer cells release certain molecules that interact with the immune system, sending out signals that favor the growth and spread of tumors.

In the future, the researchers hope that their new discovery will allow scientists to come up with better strategies for targeting aggressive melanoma and preventing a relapse.

A complex signaling mechanism

The research team looked both at melanoma tumor samples collected from human patients as well as mouse models of this form of cancer.

The investigation revealed that skin cancer's aggressiveness is largely due to the presence of the protein myosin II in large quantities within cancer cells.

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Myosin II contributes to cell motility, meaning that it helps cells move around; thus, high levels of this protein allow cancer cells to become more mobile and spread around the body quicker.

However, the researchers also found that myosin II stimulates the secretion of substances that send out signals to the immune system, "telling" it to bypass cancer cells.

More specifically, these substances "speak" to macrophages. These are specialized immune cells that normally consume and eliminate foreign bodies, malfunctioning cells, and cellular debris.

When these macrophages receive the signals from the melanoma cells — due to the action of myosin II — this "programs" them to avoid attacking cancer tumors, letting them grow and spread freely.

Targeting the chemical culprits

Another effect of the substances secreted thanks to myosin II is the puncturing of blood vessels so that cancer cells can pass into the bloodstream and travel to distant sites inside the body.

"This study," explains lead author Prof. Vicky Sanz-Moreno, of QMUL, "highlights how cancer cells interact with and influence their surrounding environment to grow and spread."

"Developing treatments that target the chemicals that alter the immune system," she adds, "could help to prevent the spread of the disease."

Further analyses showed the team that the most important chemical released through myosin II is interleukin 1A, a signaling protein that helped boost the invasiveness of cancer cells.

When the researchers decided to target myosin II and block its activity, cancer cells released less interleukin 1A — both in mouse models and human melanoma samples.

"By using therapeutic drugs that block either myosin II activity or the release of interleukin 1A, we can make the tumor less invasive and slow its growth, making it easier to treat."

Prof. Vicky Sanz-Moreno