Pancreatic cancer is one of the most frequent causes of cancer deaths in the U.S. today. Studies have shown this disease to be particularly difficult to treat for it is often resistant to treatment. Diagnosis is difficult for initial clinical signs are hard to detect. In this experiment, the role of nicotine in inducing a more aggressive growth progression of pancreatic cancer cells was analyzed through BrdU, invasion and wound healing assays. The findings suggest the nicotine drug may be responsible for further mitotic cell cycle progression and cell cycle regulation.

Recent studies have shown that nicotine, which is not a carcinogen, can stimulate a more rapid proliferation rate in cancer cells. Nicotine may mediate pro survival pathways in cancers promoting the growth of solid tumors in vivo through nicotinic acetylcholine receptor signaling pathways which first mediates through Src activation. Analysis of human pancreatic cancer cells show enhanced growth rates when stimulated with 1 µM nicotine.

BrdU incorporation assays indicated that 1 µM nicotine stimulated cell cycle progression into S-phase entry for AsPC-1 and Line-1 cells. Inhibitors such as LY-294002, PP2, UO126, HexBr and 251 were observed to inhibit nicotine induced S-phase entry in AsPC-1 and Line-1 cells. The effect of each inhibitor in nicotine’s signaling pathway is discussed. Wound healing and directional cell migration were evaluated. Nicotine stimulation caused a more rapid rate of migration. It appears that nicotine induces cell proliferation through its nicotinic acetylcholine receptors and directly stimulates cell proliferation and further spread of pancreatic cancer tumor cells.