Nicotine binding to the nicotinic acetylcholine receptor (nAchR) may directly promote the development of breast cancer, according to a study published online August 23 in The Journal of the National Cancer Institute.
While smoking is a well-known risk factor for a broad range of cancer types, non-nicotine components of tobacco have generally been thought to be the carcinogens. Hence little is known about how nicotine acts on cells to promote cancer cell growth. For breast cancer in particular, some large epidemiological studies have reportedly suggested that smoking is related to increased breast cancer risk, but they have not been accompanied by molecular biology studies on how that actually works.
To determine whether nicotine works on the cellular level to promote breast cancer growth, Yuan-Soon Ho, Ph.D., of Taiwan’s Taipei Medical University, and colleagues looked at 276 breast tumor samples from anonymous donors to the Taipei Medical University Hospital to see whether subunits of the nicotinic acetylcholine receptor were overexpressed in breast cancer cells compared with surrounding normal cells.
The researchers found that human breast cancer cells consistently overexpressed the alpha 9 subunit of the nAChR (α9-nAchR). That expression was higher in advanced-stage breast cancer compared with early-stage cancer. They also found that reducing the levels of α9-nAchRs inhibited tumor growth in laboratory experiments, whereas increasing the levels of α9-nAchRs or treating more normal breast cells with nicotine promoted the development of cancer characteristics.
"These results imply that receptor-mediated carcinogenic signals play a decisive role in biological functions related to human breast cancer development," the authors write. They note that their study was limited by its small sample size and the fact that it included only Asian patients. Breast cancer in Taiwan is characterized by its low incidence rate and early stage of tumor onset.