Title : Nicotine promotes proliferation of human nasopharyngeal carcinoma cells by regulating α7AChR, ERK, HIF-1α and VEGF/PEDF signaling.

Pub. Date : 2012

PMID : 22952803






6 Functional Relationships(s)
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1 Nicotine promotes proliferation of human nasopharyngeal carcinoma cells by regulating alpha7AChR, ERK, HIF-1alpha and VEGF/PEDF signaling. Nicotine mitogen-activated protein kinase 1 Homo sapiens
2 The mechanism studies showed that the observed stimulation of proliferation was accompanied by the nicotine-mediated simultaneous modulation of alpha7AChR, HIF-1alpha, ERK and VEGF/PEDF signaling. Nicotine mitogen-activated protein kinase 1 Homo sapiens
3 Nicotine also promoted the phosphorylation of ERK1/2 but not JNK and p38 proteins, thereby induced the activation of ERK/MAPK signaling pathway. Nicotine mitogen-activated protein kinase 1 Homo sapiens
4 Pretreatment with an ERK-selective inhibitor effectively reduced the nicotine-induced proliferation of NPC cells. Nicotine mitogen-activated protein kinase 1 Homo sapiens
5 Pretreatment with a alpha7AChR or ERK-selective inhibitor or transfection with a HIF-1alpha-specific siRNA in NPC cells significantly inhibited the nicotine-induced HIF-1alpha expression and VEGF/PEDF ratio. Nicotine mitogen-activated protein kinase 1 Homo sapiens
6 These results therefore indicate that nicotine promotes proliferation of human NPC cells in vitro through simultaneous modulation of alpha7AChR, HIF-1alpha, ERK and VEGF/PEDF signaling and suggest that the related molecules such as HIF-1alpha might be the potential therapeutic targets for tobacco-associated diseases such as nasopharyngeal carcinomas. Nicotine mitogen-activated protein kinase 1 Homo sapiens