To study the combined effect of THC and KSHV, the researchers examined a culture of human skin cells, which are susceptible to infection and could provide a model of Kaposis sarcoma. These culture cells display many copies of two prominent cannabinoid receptors. Dr. Groopman and his colleagues found that by bonding to these receptors, low doses of THC activate two proteins responsible for maintaining a cells internal framework, or cytoskeleton. By altering the cytoskeleton, THC effectively opens the door for KSHV, allowing the virus to more easily enter and infect the cell. We can take away that effect by using antagonists that block the two cannabinoid receptors, which adds evidence that THC is the culprit, Dr. Groopman said.

Once a cell is infected, the presence of THC may also promote the cellular events that turn it cancerous, the researchers say. They found that THC also promotes the production of a viral receptor similar to one that attracts a cell-signaling protein called interleukin-8. Previous studies have noted that this receptor could trigger the cell to reproduce, causing Kaposis sarcoma-like lesions in mice. Indeed, the researchers saw that THC induced the infected cells to reproduce and form colonies in culture.

Here we see both infection and malignancy going on in the presence of THC, offering some serious concerns about the safety of THC among those at risk, Dr. Groopman said. Of course, we still do not know the exact molecular events that are occurring here, but these results are just the first part of our ongoing research.

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Contact: Greg Lester
lester@aacr.org
267-646-0554
American Association for Cancer Research
1-Aug-2007