AI Article Synopsis
- Nicotine is a carcinogenic agent linked to gastric cancer, promoting tumor progression through disruption of epithelial-mesenchymal transition (EMT).
- Long-term nicotine exposure activates 5-lipoxygenase (5-LOX) in gastric cancer cells, leading to increased cell proliferation, invasiveness, and decreased apoptosis.
- Blocking 5-LOX signaling alters several factors associated with cancer progression and EMT, suggesting that the Erk/5-LOX pathway plays a crucial role in nicotine's effects on cancer cells.
Article Abstract
Nicotine is shown to be one of the carcinogenic agents for gastric cancer. Perturbation of epithelial-mesenchymal transition (EMT) results in loss of intracellular adhesions leading to tumor progression. In this study, we examined the underlying mechanism of the long-term effects of nicotine on tumor progression in human gastric cancer cells. Nicotine activated 5-lipoxygenase (5-LOX) in three gastric cancer cell lines (MKN-45, MKN-28 and AGS). Cells treated with nicotine dose- and time-dependently induced cell proliferation, invasion and suppressed apoptosis. In addition, cell cycle progression analysis revealed that activation of 5-LOX modulated the G1/S phase transition regulatory proteins and caused cell proliferation. MK886 (5-LOX activating protein inhibitor) mediated the induction of apoptosis by elevation of caspase-3 and Bax/Bcl2 ratio. Abrogation of 5-LOX repressed featured molecular markers of EMT (inactivation of E-cadherin and activation of transcriptional repressor Snail). Blockade of 5-LOX signaling resulted in downregulation of cyclin D1, matrix metalloproteinase (MMP-7, -9), urokinase plasminogen activator (uPA) and its receptor (uPAR), and pro-apoptotic proteins. Furthermore, suppression of Snail and induction of E-cadherin is extracellular signal-regulated kinase (Erk)-dependent. Thus, we conclude that the promotion effect of nicotine on cancer cell progression and EMT is mediated by Erk/5-LOX signaling pathway.
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| http://dx.doi.org/10.1016/j.canlet.2009.12.011 | DOI Listing |
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