ArticlePloS one2012
Nicotine promotes proliferation of human nasopharyngeal carcinoma cells by regulating α7AChR, ERK, HIF-1α and VEGF/PEDF signaling.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 69 citations in OpenAlex.
- Transcriptomic and experimental validation identify biomarkers and regulatory mechanisms associated with the aryl hydrocarbon receptor in nasopharyngeal carcinoma.Translational cancer research · 2026Article
- Nicotine-Induced VEGF Levels in NSCLC Cells Are Modulated by PKA, Hyaluronan, and p53.International journal of molecular sciences · 2025Article
- Early circulating EBV-DNA clearance predicts enhanced short-term treatment response and survival benefit in locally advanced nasopharyngeal carcinoma.BMC cancer · 2025Article
- The role of acetylcholine and its receptors in tumor immune regulation: mechanisms and potential therapeutic targets.Molecular cancer · 2025Review
- Relationship between urinary iodine concentration and all-cause mortality in individuals with diabetes: An analysis of National Health and Nutrition Examination Survey 2005 - 2018.Hormones (Athens, Greece) · 2025Article
- The angiogenic role of the alpha 9-nicotinic acetylcholine receptor in triple-negative breast cancers.Angiogenesis · 2024Article
- Predicting risk factors for Epstein-Barr virus reactivation using Bayesian network analysis: a population-based study of high-risk areas for nasopharyngeal cancer.Frontiers in oncology · 2024Article
- Angiogenesis in nasopharyngeal carcinoma: insights, imaging, and therapeutic strategies.Frontiers in oncology · 2024Review
- Non-Antigenic Modulation of Antigen Receptor (TCR) Cβ-FG Loop Modulates Signalling: Implications of External Factors Influencing T-Cell Responses.International journal of molecular sciences · 2023Article
- SHMT2 promotes tumor growth through VEGF and MAPK signaling pathway in breast cancer.American journal of cancer research · 2022Article
- Article
- Modified Snake α-Neurotoxin Averts β-Amyloid Binding to α7 Nicotinic Acetylcholine Receptor and Reverses Cognitive Deficits in Alzheimer's Disease Mice.Molecular neurobiology · 2021Article
- New Pathways for the Skin's Stress Response: The Cholinergic Neuropeptide SLURP-1 Can Activate Mast Cells and Alter Cytokine Production in Mice.Frontiers in immunology · 2021Article
- Nicotine Rescues Depressive-like Behaviors via α7-type Nicotinic Acetylcholine Receptor Activation in CaMKIV Null Mice.Molecular neurobiology · 2020Article
- A nicotine-induced positive feedback loop between HIF1A and YAP1 contributes to epithelial-to-mesenchymal transition in pancreatic ductal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2020Article
- Effects and significance of formononetin on expression levels of HIF-1α and VEGF in mouse cervical cancer tissue.Oncology letters · 2019Article
- Smoking can increase nasopharyngeal carcinoma risk by repeatedly reactivating Epstein-Barr Virus: An analysis of a prospective study in southern China.Cancer medicine · 2019Article
- VPS33B interacts with NESG1 to modulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling and induce 5-fluorouracil sensitivity in nasopharyngeal carcinoma.Cell death & disease · 2019Article
- Addition of bevacizumab to systemic therapy for locally advanced and metastatic nasopharyngeal carcinoma.Oncology letters · 2018Article
- Endothelial CaInternational journal of molecular sciences · 2018Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
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Abstract
Nicotine, the major component in cigarette smoke, can promote tumor growth and angiogenesis, but the precise mechanisms involved remain largely unknown. Here, we investigated the mechanism of action of nicotine in human nasopharyngeal carcinoma (NPC) cells. Nicotine significantly promoted cell proliferation in a dose and time-dependent manner in human NPC cells. The mechanism studies showed that the observed stimulation of proliferation was accompanied by the nicotine-mediated simultaneous modulation of α7AChR, HIF-1α, ERK and VEGF/PEDF signaling. Treatment of NPC cells with nicotine markedly upregulated the expression of α7AChR and HIF-1α proteins. Transfection with a α7AChR or HIF-1α-specific siRNA or a α7AChR-selective inhibitor significantly attenuated the nicotine-mediated promotion of NPC cell proliferation. Nicotine also promoted the phosphorylation of ERK1/2 but not JNK and p38 proteins, thereby induced the activation of ERK/MAPK signaling pathway. Pretreatment with an ERK-selective inhibitor effectively reduced the nicotine-induced proliferation of NPC cells. Moreover, nicotine upregulated the expression of VEGF but suppressed the expression of PEDF at mRNA and protein levels, leading to a significant increase of the ratio of VEGF/PEDF in NPC cells. Pretreatment with a α7AChR or ERK-selective inhibitor or transfection with a HIF-1α-specific siRNA in NPC cells significantly inhibited the nicotine-induced HIF-1α expression and VEGF/PEDF ratio. These results therefore indicate that nicotine promotes proliferation of human NPC cells in vitro through simultaneous modulation of α7AChR, HIF-1α, ERK and VEGF/PEDF signaling and suggest that the related molecules such as HIF-1α might be the potential therapeutic targets for tobacco-associated diseases such as nasopharyngeal carcinomas.
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