Cigarette smoking is a recognized risk factor for colon cancer and nicotine, the principal active component of tobacco, plays a pivotal role in increasing colon cancer cell growth and survival. The aim of this study was to determine the effect of nicotine on cellular Caco-2 and HCT-8 migration and invasion, focusing on epithelial to mesenchymal transition (EMT) induction, and COX-2 pathway involvement. In both these cell lines, treatment with nicotine increased COX-2 expression and the release of its enzymatic product PGE2. Moreover, nicotine-stimulated cells showed increased migratory and invasive behavior, mesenchymal markers up-regulation and epithelial markers down-regulation, nuclear translocation of the β-catenin, increase of MMP-2 and MMP-9 activity, and enhanced NF-κB expression. Noticeably, all these effects are largely mediated by COX-2 activity, as simultaneous treatment of both cell lines with nicotine and NS-398, a selective COX-2 inhibitor, greatly reduced the number of migrating and invading cells and reverted nicotine-induced EMT. These findings emphasize that nicotine triggers EMT, leading hence to increased migration and invasiveness of colon cancer cells. Thereby, the use of COX-2 inhibitor drugs might likely counteract nicotine-mediated EMT effects on colon cancer development and progression

Nicotine increases colon cancer cell migration and invasion through epithelial to mesenchymal transition (EMT): COX-2 involvement / Dinicola, Simona; Masiello, Maria G.; Proietti, Sara; Coluccia, Pierpaolo; Fabrizi, Gianmarco; Catizone, Angela; Ricci, Giulia; de Toma, Giorgio; Bizzarri, Mariano; Cucina, Alessandra. - In: JOURNAL OF CELLULAR PHYSIOLOGY. - ISSN 0021-9541. - 233:6(2018), pp. 4935-4948. [10.1002/jcp.26323]

Nicotine increases colon cancer cell migration and invasion through epithelial to mesenchymal transition (EMT): COX-2 involvement

Dinicola, Simona;Masiello, Maria G.;Proietti, Sara;Coluccia, Pierpaolo;Fabrizi, Gianmarco;Catizone, Angela;de Toma, Giorgio;Bizzarri, Mariano;Cucina, Alessandra
2018

Abstract

Cigarette smoking is a recognized risk factor for colon cancer and nicotine, the principal active component of tobacco, plays a pivotal role in increasing colon cancer cell growth and survival. The aim of this study was to determine the effect of nicotine on cellular Caco-2 and HCT-8 migration and invasion, focusing on epithelial to mesenchymal transition (EMT) induction, and COX-2 pathway involvement. In both these cell lines, treatment with nicotine increased COX-2 expression and the release of its enzymatic product PGE2. Moreover, nicotine-stimulated cells showed increased migratory and invasive behavior, mesenchymal markers up-regulation and epithelial markers down-regulation, nuclear translocation of the β-catenin, increase of MMP-2 and MMP-9 activity, and enhanced NF-κB expression. Noticeably, all these effects are largely mediated by COX-2 activity, as simultaneous treatment of both cell lines with nicotine and NS-398, a selective COX-2 inhibitor, greatly reduced the number of migrating and invading cells and reverted nicotine-induced EMT. These findings emphasize that nicotine triggers EMT, leading hence to increased migration and invasiveness of colon cancer cells. Thereby, the use of COX-2 inhibitor drugs might likely counteract nicotine-mediated EMT effects on colon cancer development and progression
2018
Colon cancer; COX-2; EMT; invasion; migration; nicotine; physiology; clinical biochemistry; cell biology
01 Pubblicazione su rivista::01a Articolo in rivista
Nicotine increases colon cancer cell migration and invasion through epithelial to mesenchymal transition (EMT): COX-2 involvement / Dinicola, Simona; Masiello, Maria G.; Proietti, Sara; Coluccia, Pierpaolo; Fabrizi, Gianmarco; Catizone, Angela; Ricci, Giulia; de Toma, Giorgio; Bizzarri, Mariano; Cucina, Alessandra. - In: JOURNAL OF CELLULAR PHYSIOLOGY. - ISSN 0021-9541. - 233:6(2018), pp. 4935-4948. [10.1002/jcp.26323]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1079028
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