U.S. scientists have discovered a molecular mechanism that found an important role in the development of malignant tumors in the lung under the influence of tobacco smoke. According to researchers, the most likely cause of malignant transformation of bronchial epithelial cells a disabling FANCD2 gene, responsible for the destruction of cancer cells and repair damaged DNA. The conditions in the development of the smoker reproduce lungs, bronchial epithelial cells, the researchers placed in a hollow tube, through which the smoke. As it turned out, decreased the effects of tobacco smoke condensate, the activity of the gene in the cells of FANCD2. Protein, which is encoded by this gene is a component of the protein complex for the maintenance of the structure of DNA and cell killing mutants. With a lack of FANCD2 into cells, the number of chromosomal mutations, and then dissolved in normal cells to programmed cell death - apoptosis. Under the influence of tobacco smoke, and increased the number of mutations in the cell lines of malignant lung tumors, but this does not lead to self-destruction of cells, and they continue to actively proliferate. According to the authors, smoking can have a similar effect on the synthesis of other proteins. For the maintenance of DNA However, the compelling evidence for the key role of FANCD2 in the development of lung cancer in smokers is protected by the fact that the cells with a high content of proteins completely from the harmful effects of tobacco smoke. The report on the study in the latest issue of the British Journal of Cancer published.
No comments:
Post a Comment