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Nicotine binding to receptor linked to breast cancer cell growth

Date:
August 24, 2010
Source:
Journal of the National Cancer Institute
Summary:
When nicotine binds to the nicotinic acetylcholine receptor (nAchR), it is known to promote smoking addiction and may also directly promote the development of breast cancer, according to a new study.

When nicotine binds to the nicotinic acetylcholine receptor (nAchR), it is known to promote smoking addiction and may also directly promote the development of breast cancer, according to a study published online August 23 in The Journal of the National Cancer Institute.

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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, so little is known about how nicotine acts on cells to promote cancer cell growth. For breast cancer in particular, some large epidemiological studies have 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 the 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), and 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.

The authors write: "These results imply that receptor-mediated carcinogenic signals play a decisive role in biological functions related to human breast cancer development."

The authors say 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.

In an accompanying editorial, Ilona Linnoila, M.D., of the Center for Cancer Research at the National Cancer Institute, writes that the study "suggests not only that smoking could be causally related to breast carcinogenesis but also that nicotine could directly contribute to the molecular mechanism of carcinogenesis in addition to indirectly contributing by promoting addiction to smoking."

Furthermore, Linnoila writes, "Better understanding of the molecular mechanisms of the cholinergic pathways will lead to more opportunities for intervention and prevention of tobacco toxicity."


Story Source:

The above story is based on materials provided by Journal of the National Cancer Institute. Note: Materials may be edited for content and length.


Journal Reference:

  1. Chia-Hwa Lee, Ching-Shui Huang, Ching-Shyang Chen, Shih-Hsin Tu, Ying-Jan Wang, Yu-Jia Chang, Ka-Wai Tam, Po-Li Wei, Tzu-Chun Cheng, Jan-Show Chu, Li-Ching Chen, Chih-Hsiung Wu, and Yuan-Soon Ho. Overexpression and Activation of the α9-Nicotinic Receptor During Tumorigenesis in Human Breast Epithelial Cells. Journal of the National Cancer Institute, 2010; DOI: 10.1093/jnci/djq300

Cite This Page:

Journal of the National Cancer Institute. "Nicotine binding to receptor linked to breast cancer cell growth." ScienceDaily. ScienceDaily, 24 August 2010. <www.sciencedaily.com/releases/2010/08/100823162320.htm>.
Journal of the National Cancer Institute. (2010, August 24). Nicotine binding to receptor linked to breast cancer cell growth. ScienceDaily. Retrieved March 31, 2015 from www.sciencedaily.com/releases/2010/08/100823162320.htm
Journal of the National Cancer Institute. "Nicotine binding to receptor linked to breast cancer cell growth." ScienceDaily. www.sciencedaily.com/releases/2010/08/100823162320.htm (accessed March 31, 2015).

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