Nicotine may spur the spread of breast cancer, pushing cells from the original tumor to other parts of the body, said a study published in the latest issue of Cancer Research, a journal of the American Association for Cancer Research.
Although scientists need time to pinpoint the exact role nicotine may play in breast cancer's spread, there is no doubt that nicotine may contribute to the metastasis that so often kills patients, according to the study published earlier this month.
Besides serving as yet another warning against smoking, the finding may also point to new targets for cancer drugs, said the study conducted by researchers at Beth Israel Deaconess Medical Center and Harvard Medical School, Boston.
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," said Dr. Chang Yan Chen, from the department of radiation oncology, who took part in the study.
"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."
Therefore, while much of the research on nicotine has focused on its effects on the neural system, recent research indicates that nicotine can also activate signaling pathways in non-neuronal cells, including tumor cells, said the study.
In a series of lab experiments, Chen and his 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 study showed. The findings were confirmed in mice.
Nicotine does 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."
(Xinhua News Agency October 20, 2008)
