VEGF and carcinogens in lung cancer

Nicotine and estradiol promote VEGF secretion by NSCLC tumors

Jarzynka et al investigated the effect of nicotine on lung cancer cells in a preclinical study. This image shows VEGF expression in mice with lung tumors in: a) control group; b) nicotine-treated; c) estradiol-treated; and d) nicotine- and estradiol-treated A549 non-small cell lung cancer (NSCLC) tumors.¹

Reprinted from Int J Oncol. Vol 28. Jarzynka MJ, Guo P, Bar-Joseph I, Hu B, Cheng SY. Estradiol and nicotine exposure enhances A549 bronchioloalveolar carcinoma xenograft growth in mice through the stimulation of angiogenesis. Pages 337-344. © 2006. Reproduced with permission from copyright holder.

Lung cancer is strongly linked to a known carcinogen—tobacco smoking. Preclinical research indicates that expression of vascular endothelial growth factor (VEGF) may be one way in which cells react to nicotine, a component of tobacco. Jarzynka and colleagues studied the exposure of mice with xenograft bronchioloalveolar carcinoma to estradiol, nicotine, or both. Mice exposed to both estradiol and nicotine developed significantly larger tumors than control animals, and their tumors had significantly higher increases in microvessel density. Mice exposed to nicotine alone demonstrated higher microvessel density as well, but this difference was not statistically significant. As stated by the investigators, "These results suggest that estradiol and nicotine may act in concert to stimulate angiogenesis in vivo." As with microvessel density, VEGF expression was also shown to correlate with exposure to estradiol and nicotine together. Individually, nicotine increased VEGF expression slightly, while a greater increase was seen with estradiol alone. The clinical significance of these findings is unknown.¹

Reference:

1.

Jarzynka MJ, Guo P, Bar-Joseph I, Hu B, Cheng SY. Int J Oncol. 2006;28:337-344.