【Animal Modeling】-Drosophila model reveals cancer consumption mechanism

  The gradual loss of muscle and adipose tissue throughout the body is one of the most obvious and painful clinical manifestations of cancer, but no one knows how it degenerates distant tissues. A molecule called ImpL2 secreted by cancer may cause the loss of fat and muscle tissue in fruit flies. These findings have led to more targeted treatments for wasting syndrome in cancer patients.

  "Many cancer patients die not from the local effects of cancer, but from the broader and systemic changes caused by cancer. The most serious of these long-term effects is syndrome or cachexia wasting, which is part of cancer treatment. Important diseases," said David Bilder, a developmental biologist at the University of California, Berkeley. tell. Approximately 20% of cancer deaths are caused by wasting syndrome, which mainly affects patients with advanced cancer who are too weak to receive certain chemotherapy or radiotherapy, making them vulnerable to the side effects of chemotherapy. Do it. Increasing food intake cannot reverse the loss of tissue, and the treatments available are very limited.

  In order to change the status quo, two independent research groups have developed effective genetic methods. The fruit fly model they created can quickly identify consumption inducements similar to cachexia. A team of builders transplanted tumor cells into the abdomen of Drosophila and induced Drosophila cancer. Another team led by Nobert Perimon of Harvard Medical School activated the Yorkie protein to grow cancer cells in the intestinal stem cells of fruit flies. In both cancer models, the researchers found that a cancer-secreting molecule called ImpL2 causes fruit flies to consume fat, muscle and ovaries. They found that reduced ImpL2 levels can effectively delay fruit fly waste syndrome.

  These studies also raise another interesting question. How can the growing tumor avoid the impact of ImpL2? One of the clues discovered by Perrimon et al. is that insulin signals in the gut and distant tissues are inconsistent with glucose metabolism. Compared with muscle and ovary, intestinal stem cell proliferation increases insulin signaling and increases the level of enzymes produced by glycolysis. Because ImpL2 depletion cannot fully restore tissue loss, researchers are also looking for other factors that affect Drosophila cancer wasting syndrome.