Compound inhibited receptors and led to cancer cell death in mouse study
MONDAY, June 15 (HealthDay News) -- In a study of mice with lung cancer, a treatment that targeted nicotine receptors more than doubled the animals' survival time, Italian researchers say.
Nicotine plays a dual role in lung cancer. Changes in genes encoding nicotine receptors not only drive the urge the smoke, but also increase susceptibility to lung cancer. Exposure to nicotine boosts the expression of nicotine receptors, which leads to increased cell proliferation and inhibits the programmed cell death known as apoptosis.
In the new study, published in the June 15 issue of the American Journal of Respiratory and Critical Care Medicine, the compound α-CbT dampened the expression of nicotine receptors and increased apoptosis, prolonging the lives of the mice.
"This research clearly has profound clinical implications regarding the role of nicotine in stimulating lung cancer and nicotine receptor antagonists in treating the disease," said Dr. John Heffner, past president of the American Thoracic Society, in a news release from the society. Heffner, who was not involved in the research, added, "The highly addictive nature of nicotine, however, complicates patients' ability to quit smoking and avoid ongoing nicotine exposure."
Previous research has shown that it's possible to dampen the response of nicotine acetylcholine receptors (nAChRs) using an antagonist called d-tubocurarine/α-Cobratoxin (α-CbT), which specifically targeted the area most linked to increased cell growth.
In the study, researchers grafted human non-small-cell lung carcinoma (NSCLC) onto the lungs of mice and then delayed treatment, allowing the tumors to become well-established.
The mice were then divided into three groups: the untreated group; the standard chemotherapy drug group; and the α-CbT group.
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