2017年3月17日星期五

Cancer cells may spread faster due to fat metabolism

Hepatocarcinoma is the third leading cause of cancer-related death worldwide and is the fastest growing cancer in Australia. "Many people suspect that the fatal nature of liver cancer is the process of cell metabolism, which is thought to play an important role in helping cancer cells to proliferate," says Kyle Hoehn, associate professor at UNSW. The team led by Hoehn managed to successfully prevent the formation of fat in hepatocytes of transgenic mice with unintended consequences. Unlike the team predicted that the termination of the growth of cancer cells, blocking this metabolic pathway led to more than twice the emergence of the tumor. The surprising results were published this week in Nature Communications, which also publishes other studies on recombinant human proteins.

Hoehn said, "It is currently developing drugs to target and block this metabolic pathway, which is considered promising to treat the liver and other cancers. These results may cause some concern at least for liver cancer. Our findings are completely contrary to intuition. But it is clear that any use of these drugs in the treatment of liver cancer should be more cautious in the future because there may be unintended consequences."

When cells divide, they need to reconstruct all of their structural components including their protective film made of fat and promote the process through lipid production. "The fat generation is the hallmark of invasive liver cancer, and the survival rate of high-fat-producing tumors is the lowest," Hoehn said. "Before we start this experiment, we believe that if you can knock out fat-producing legs, then you can stop rapid formation or proliferation of cancer cells."

The team tested whether their genetically-modified mice could obtain cancer by exposure to DNA-damaging carcinogens and introducing high-fat diets. These injuries increase the risk of developing advanced tumors of life. At 9 months of age, they compared the tumor burden of genetically-modified mice and mice with normal liver fat production. The results were very surprising. In addition, the team found that cancer cells rapidly adapt to the loss of fat production: they began to remove more fat from the blood and burn more fat by burning less fat. Thus, by pulling out one leg of lipid metabolism, they got stronger.

Although it looks like a retrograde on the surface of cancer treatment, Hoehn said, "Cancer cells seem to always have a solution. They are smart little bastards. This finding has revealed valuable insights into the complex biology of cancer cells and also identifies possible new targets for future drugs: mechanisms that drive antioxidant defense systems or fat intake." By the way, Flarebio offers high-quality recombinant proteins such as recombinant NPP1 for your research.

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