beta erythroidine/悪性腫瘍

Cigarette smoking is not only a documented risk for lung carcinogenesis but also promotes lung cancer development. Nicotine, a major component of cigarette smoke but not a carcinogen by itself, has been found to induce proliferation, invasion and metastasis of non-small cell lung cancer (NSCLC).

It was demonstrated that nicotine increased non-small cell lung cancer cell proliferation through nicotinic acetylcholine receptor -mediated signals. However, the detailed mechanism remains incompletely understood. We evaluated whether nicotine increased EP4 receptor expression in lung carcinoma

A pharmacological analysis was made of the depolarizing acetylcholine (ACh) response found on the gastric mill I muscles of the crabs Cancer pagurus, Cancer irroratus and Cancer borealis. Acetylcholine, carbamylcholine, trimethylammonium, nicotine, and dimethyl-4-phenyl-piperazinium were effective

Non-small cell lung cancer (NSCLC) demonstrates a strong etiologic association with smoking. Although nicotine is not carcinogenic, it can induce cell proliferation and angiogenesis and suppress apoptosis induced by certain agents. Here we show that nicotine inhibits apoptosis induced by the drugs