Washington, Oct 15 : Researchers at the Beth Israel Deaconess Medical Center suggest a possible role for nicotine in breast tumor development and metastases.
The study is the first of its kind to explore the effects of nicotine on mammary cells.
"Although numerous studies indicate the role of nicotine exposure in tumor promotion, little is known about the effect of nicotine on breast tumor development, especially on the metastatic process of breast cancer," said lead author Chang Yan Chen, Ph.D., M.D., at Beth Israel Deaconess Medical Center.
After conducting a series of in vitro tests, researchers found that breast epithelial-like MCF10A cells and cancerous MCF7 cells both express several subunits of nAChR (nicotine receptor).
When bound, nAChR initiate a signaling process, potentially increasing cell growth and migration.
"The best known role of nAChR is in the nerve system. Although cells from various tissue origins express different subunits of nAChR, we know very little about the functions of nAChR in non-neuronal cells and tissues, in particular in mammary cells," said Chen.
He added: "We were able to determine that mammary cells express different subunits of nAChR and that nicotine, possibly through perturbing cell cycle checkpoints, potentiates tumorigenesis in mammary cancer-prone or cancer cells."
The findings were confirmed via In vivo studies.
After the cancerous MCF7 cells were injected into the tail of a mouse, they migrated to the lungs.
The in vivo and in vitro studies indicated that nicotine is not a conventional carcinogen, but it combines with other yet to be determined factors to enable tumorigenesis.
"In vitro and in vivo tests showed that no metastasis occurs when the administration of nicotine alone. At this point we can only suggest that nicotine potentiates the growth-related process," said Chen.
The study is published in Cancer Research, a journal of the American Association for Cancer Research.