Exposure to nicotine from cigarettes you smoke and from second-hand smoke from other people's cigarettes has been linked to cancer and serious respiratory and heart diseases. The basic research study reviewed here found that nicotine made normal and cancerous breast cell cultures grow and spread. Breast cancer cells are identified by abnormal growth and their ability to spread -- both within the breast and to other parts of the body. So the researchers think that these results might explain why nicotine exposure from second-hand smoke can promote breast cancer.
Basic research involves cell cultures in a lab. No people participated in this study.
Even though nicotine doesn't naturally occur in people, human cells have nicotine receptors, called nicotine acetylcholine receptors (nAChR). When nicotine attaches to these receptors in the nerves of the brain, it triggers an addiction to nicotine that makes quitting smoking very, very difficult.
In this study, nicotine attached to the nAChR receptors on breast cells, causing chemical signals that are known to promote the growth and spread of cells.
These results add to evidence that cigarette smoking and exposure to second-hand smoke are dangerous to your health, including breast health. The risk to your health may be even greater if you've already been diagnosed with breast cancer. Nicotine exposure increases your risk of developing another breast cancer in the future.
If you don't smoke but are exposed to nicotine by other smokers, do all you can to avoid their smoke. And do your best to encourage them to quit -- for your sake and theirs. If you do smoke, quit. Yes, it's very hard to stop smoking. But quitting is something you can do that can make a huge difference in your health and well-being, now and in the future. Help quitting is available:
Visit the Breastcancer.org Lower Your Risk section to learn more about how you or someone you care about can quit smoking for good.
BOSTON, Oct. 15 (MedPage Today) -- Nicotine from even second-hand cigarette smoke may stimulate breast cancer tumorigenesis and progression by interacting with receptors in tissue to signal cell growth and migration, laboratory studies here suggested.
In malignant and breast epithelial cells, exposure to nicotine enhanced the activity of a tumor-promoting enzyme and stimulated the cells' mobility, Chang Yan Chen, M.D., Ph.D., of Harvard, and colleagues reported in the Oct. 15 issue of Cancer Research.
The studies also identified a cell division cycle gene that appears to play a key role in nicotine-mediated cell migration.
Moreover, the data suggest a possible mechanism by which second-hand smoking may lead to tumorigenesis.
"Together, our findings suggest that nicotine, through interacting with its receptor, initiates a signaling cascade . . . and consequently promotes migration in mammary epithelial or tumor cells," the authors concluded.
"Overall, our study provides evidence to suggest that nicotine is a possible component for initiation of breast cancer induced by second-hand smoking," they added. "The present investigation also warrants a caution for the clinical use of nicotine to relieve chronic pain or aid in the cessation of cigarette smoking."
The nicotine acetylcholine receptor (nAChR) has a well recognized role in neuronal activity associated with nicotine addiction. More recently, nicotine has been shown to activate intracellular signaling pathways in non-neuronal cells, suggesting potential involvement in tumor development, the authors said.
"After engaging its receptor, nicotine rapidly activates mitogenic-related, intracellular signaling pathways in endothelial cells or keratinocytes," they wrote. "Emerging evidence showed that nicotine potentially induces secretion of different types of [proteases] from lung cancer cells, which then promotes cleavage of various substrates in the extracellular matrix to facilitate metastasis and tumor progression."
Numerous studies have shown nicotine exposure in tumorigenesis, but little is known about the effect of nicotine on development and metastasis of breast cancer, the authors continued.
In the current study, the authors examined signaling pathways by which nicotine might promote tumor development and progression in the breast, using human breast epithelial-like MCF10A cells and MCF7 cancer cells.
The authors found that MCF10A and MCF7 cells express four nAChR subunits. Exposure to nicotine increased the activity of protein kinase C (PKC)-alpha without altering expression of the protein.
The authors reported that nicotine stimulated [3H]thymidine incorporated into the genome of the cells and forced serum-starved cells to enter S-phase of the cell cycle, leading to growth promotion.
Nicotine exposure also increased MCF10A and MCF7 mobility, which could be inhibited by nAChR or a PKC inhibitor.
Additional laboratory studies showed that cell division cycle 42 (cdc42) functions as a downstream effector of PKC and a key regulator of nicotine-mediated cell migration.
"We showed in this study that nicotine exposure is moderately mitogenic in serum-starved MCF10A and MCF7 cells," the authors said. "Furthermore, nicotine treatment, via simulating PKC and cdc42 signaling cascade, promotes cell migration and invasion."
"We conclude that one way for nicotine to promote breast tumor development may be through potentiating metastasis," they added.
The authors reported no conflicts of interest.
Primary source: Cancer Research Source reference: Guo J, et al "Nicotine promotes mammary tumor migration via a signaling cascade involving proein kinase C and cdc42" Cancer Res 2008; 68: 8473-8481.
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