Cooperation with the occupiers
Cancerous tumors were able to exploit healthy cells
A group of scientists from the Institute of Cancer Research and the University of Manchester found that cancer cells are able to force healthy cells to help their reproduction. To do this, they use a mutated gene responsible for cell division. The results are published in the journal Cell (Tape et al., Oncogenic KRAS Regulates Tumor Cell Signaling via Stromal Reciprocation – VM). The press release of Cancer cells turn healthy cells to the 'dark side' is available on the EurekAlert website!
The researchers studied communication networks between pancreatic cancer cells – ductal adenocarcinoma. This form of cancer is responsible for nine thousand deaths in the UK every year. Scientists have studied about a thousand different compounds responsible for growth, including enzymes, receptors and signaling molecules.
The results showed that the defective version of the KRAS gene, which normally participates in the mechanism of cell division, affects not only malignant, but also healthy cells. Mutation in KRAS contributes to the hyperactivity of the gene and, as a result, uncontrolled cell growth. KRAS mutates in 90 percent of pancreatic cancer cases and in 20 percent of all cancer cases. At the same time, as it turned out, the gene sends signals to healthy cells to produce growth factors that the tumor itself cannot produce.
The tumor consists of different types of cells. One group is "spoiled" cells, the other consists of normal cells forming connective tissue (stromal cells). It is the latter who become involved in an intricate network of signaling interactions, become "hostages" of cancer and help its growth and formation of metastases.
According to scientists, research on how this network works, as well as decoding individual signals, will help in figuring out the mechanisms for controlling tumor growth and its spread throughout the body. Blocking the mutated KRAS gene may contribute to the creation of effective cancer treatments.
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15.04.2016