Smoking contributes to the vast majority (around 85 percent) of lung cancer cases. The TGF-beta signaling pathway – which regulates cell growth and proliferation – is altered in several cancer types, but little is known about how smoking affects this pathway.
To investigate this, doctoral student Debangshu Samanta, Pran Datta, associate professor of surgery, and colleagues exposed human lung epithelial cells (cells that line the airways) and lung cancer cells to low doses of “cigarette smoke condensate,” or “CSC,” for nearly one year.
They found that chronic CSC exposure decreased expression of Smad3 (a component of the TGF-beta pathway), reduced cell death, increased cell viability and enhanced tumor-forming capacity. These effects could be reversed by replacing Smad3 or withdrawing CSC. In human tumors, Smad3 expression was lower in those of current smokers compared to tumors of never-smokers.
The study, featured on the cover of the March Cancer Prevention Research, suggests that the decrease in Smad3 expression may represent a potential biomarker for smoking-induced lung cancer risk.
The research was supported by grants from the National Cancer Institute of the National Institutes of Health and the Department of Veterans Affairs.
