Nicotine May Spur Breast Cancer's Spread

By Amanda Gardner
18 oct 2008-- Nicotine may help push breast cancer cells from the original tumor to other parts of the body, contributing to the metastasis that so often kills patients.
Besides serving as yet another warning against smoking, the finding may also point to new targets for cancer drugs. However, the study's lead author stressed it is still too early to pinpoint the exact role nicotine may play in breast cancer's spread.
"I don't know what the potential is," said Dr. Chang Yan Chen, of the department of radiation oncology at Beth Israel Deaconess Medical Center and Harvard Medical School, Boston.
"This adds to the whole body of literature on how things that we ingest could potentially be harmful in terms of causing breast cancer or making existing breast cancer worse," added Dr. Julian Kim, a breast cancer surgeon and chief of oncologic surgery at University Hospitals Case Medical Center in Cleveland.
The findings were published in the Oct. 15 issue of Cancer Research.
Nicotine, a component of tobacco, has been connected with a variety of malignancies -- not only lung cancer, but also head and neck cancer, prostate cancer, and more.
"It has been known that there are 10 to 12 nicotine receptors that express on the surface of various cells," Chen explained. "We do not know why nicotine receptors express in all the cell surfaces from various tissue origins, but we do know that nicotine is an important neuron transmitter in the central nervous system. It has been reported that nicotine can promote certain intra-cellular signaling in lung cancer."
So, while much of the research on nicotine has focused on its effects on the body's nervous system, recent research indicates that nicotine can also activate signaling pathways in non-neuronal cells, including tumor cells.
In a series of lab experiments, Chen and colleagues discovered that certain breast epithelial-like cells produce different subtypes of the nicotine receptor nAChR, as do certain breast tumor cells.
When these receptors were bound with nicotine, they started signaling the cells to grow and migrate. The findings were confirmed in mice.
Nicotine did not appear to be enough to spur tumor migration on its own, although scientists don't yet know which molecules nicotine partners with to do so.
"I took two cell lines and checked to see if the cells expressed the nicotine receptor, and I found they did," Chen said. "I found that certain signaling is upregulated, but [nicotine] itself cannot push the cell to undergo tumorigenesis [cancer formation]. The conclusion is, it probably can activate a certain intracellular signaling, but really, it depends on an individual's genetic background."
"Nicotine had some effects on these tumor cells that could eventually be harmful to a patient," Kim added. "It made breast cancer cells grow more vigorously. It made them have a higher capacity to become invasive, and it made cells that are sort of precancerous turn in a direction towards cancer."