Feb. 7, 2017 / 11:05 AM
Potential breakthrough in melanoma research
A new study has identified the method melanoma cells use to spread, which could open up new treatment possibilities.
Amy Wallace
A melanoma tumor generated in the laboratory by a QUT-led research team. Researchers have identified the way melanoma cells spread, which could lead to future treatments of the disease. Photo by Dr. Aaron Smith/QUT
Feb. 7 (UPI) -- Researchers at Queensland University of Technology, or QUT, in Australia have discovered the way in which melanoma cells spread throughout the body.
The breakthrough could open up new methods to treatment by turning off the gene that causes melanoma to spread.
"Cancer is characterized by uncontrolled growth of cells but if uncontrolled growth was the only problem then cancer cells would be easily treated with surgery in most cases," Dr. Aaron Smith from QUT's School of Biomedical Sciences in the Institute of Health and Biomedical Innovation at the Translational Research Center and author of the study, said in a press release. "What makes cancer deadly is its tendency to invade tissue and migrate to other regions of the body, a process we call metastasis. Metastatic melanoma is one of the most aggressive and difficult to treat of all cancer types."
The research team, which collaborated on the study with researchers from the University of Queensland, QIMR Berghofer Medical Research Institute and Oxford University, examined melanoma tumor cells and found that some cells are primarily proliferative and some are more invasive and migratory.
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The research also found that melanoma cells can switch between the two behaviors, meaning a cell that can create a tumor can switch to facilitate the spread of the tumor to other parts of the body.
"What we did not know though was the reason why this happened," Smith said. "Our research project has discovered the mechanisms by which those melanoma cells switch behaviors."
Smith and his team found that the change in behaviors was marked by the expression of two different regulatory factors, MITF for proliferating cells and BRN2 for invasive cells.
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"BRN2 function reduces MITF expression to slow down proliferation and put the cells into invasive mode," Smith said. "Our project has identified a pathway that allows BRN2 to do this, firstly by increasing the expression of another regulatory factor called NFIB that further controls an invasive program in these cells. An important target of NFIB is an enzyme called E2H2 which then produces global [wide ranging] changes to the cells activity."
The study found that E2H2 gravitates toward the expression of invasive genes and turns off MITF to prevent proliferation.
"Once cells migrate away from the tumor we believe they no longer receive the signal that triggered the switch so the system re-sets to the MITF driven proliferation state which will then allow a new tumor to form at the new site."
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Smith said the research could lead to a drug target and allow researchers to prevent the switch to invasive behavior and the spread of melanoma cells.
The study was published in EBiomedicine.