Another link between smoking and lung cancer

American scientists have established a molecular mechanism that plays a key role in the development of malignant neoplasms in the lungs under the influence of tobacco smoke. According to researchers, the most likely cause of malignant degeneration of bronchial epithelial cells is the deactivation of the FANCD2 gene, responsible for the destruction of cancer cells and the restoration of damaged DNA.

To reproduce the conditions that develop in the lungs of a smoker, the researchers placed bronchial epithelial cells in a hollow tube through which tobacco smoke was passed. As it turned out, exposure to tobacco smoke condensation led to a decrease in the activity of the FANCD2 gene in cells.

The protein encoded by this gene is an integral part of the protein complex responsible for preserving the DNA structure and destroying mutant cells. With a lack of FANCD2 in the cells, the number of chromosomal mutations increased, after which the mechanism of programmed death – apoptosis - was triggered in healthy cells.

Under the influence of tobacco smoke, the number of mutations increased in the colonies of lung cancer cells, but this did not lead to the self-destruction of such cells, and they continued to multiply actively.

According to the authors of the study, smoking can have a similar effect on the synthesis of other proteins responsible for DNA preservation. However, the most compelling evidence of the key role of FANCD2 in the development of lung cancer in smokers is the fact that cells with an increased content of this protein remained completely protected from the harmful effects of tobacco smoke.

The research report is published in a new issue of the British Journal of Cancer.