ArticleInternational journal of cancer2009
Induction of osteopontin expression by nicotine and cigarette smoke in the pancreas and pancreatic ductal adenocarcinoma cells.
Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Acetylcholine Sustains LNCaP Prostate Cancer Cell Migration, Invasion and Proliferation Through Glyoxalase 1/MG-H1 Axis with the Involvement of Osteopontin.International journal of molecular sciences · 2025Article
- Osteopontin: an indispensable component in common liver, pancreatic, and biliary related disease.Journal of cancer research and clinical oncology · 2024Review
- Cigarette smoke-promoted increases in osteopontin expression attract mesenchymal stem cell recruitment and facilitate lung cancer metastasis.Journal of advanced research · 2022Article
- Role of the parasympathetic nervous system in cancer initiation and progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Review
- Effect of Hypercapnia, an Element of Obstructive Respiratory Disorder, on Pancreatic Cancer Chemoresistance and Progression.Journal of the American College of Surgeons · 2020Article
- High Glucose Accelerates Cell Proliferation and Increases the Secretion and mRNA Expression of Osteopontin in Human Pancreatic Duct Epithelial Cells.International journal of molecular sciences · 2017Article
- Nicotinic acetylcholine receptors and cancer.Biomedical reports · 2016Article
- The Role of nAChR and Calcium Signaling in Pancreatic Cancer Initiation and Progression.Cancers · 2015Review
- SIBLINGs and SPARC families: their emerging roles in pancreatic cancer.World journal of gastroenterology · 2014Review
- Osteopontin splice variant as a potential marker for metastatic disease in pancreatic adenocarcinoma.Journal of gastroenterology and hepatology · 2014Article
- RAN GTPase and Osteopontin in Pancreatic Cancer.Pancreatic disorders & therapy · 2013Article
- Interplay between smoking-induced genotoxicity and altered signaling in pancreatic carcinogenesis.Carcinogenesis · 2012Review
- Beta-adrenergic signaling in the development and progression of pulmonary and pancreatic adenocarcinoma.Current cancer therapy reviews · 2012Article
- Mechanisms for nicotine in the development and progression of gastrointestinal cancers.Translational gastrointestinal cancer · 2012Article
- Nicotine induces pro-inflammatory response in aortic vascular smooth muscle cells through a NFκB/osteopontin amplification loop-dependent pathway.Inflammation · 2012Article
- Pancreatic cancer cells and normal pancreatic duct epithelial cells express an autocrine catecholamine loop that is activated by nicotinic acetylcholine receptors α3, α5, and α7.Molecular cancer research : MCR · 2012Article
- Regulation of pancreatic cancer by neuropsychological stress responses: a novel target for intervention.Carcinogenesis · 2012Article
- Tumor-specific expression and alternative splicing of the COL6A3 gene in pancreatic cancer.Surgery · 2011Article
- Nicotinic acetylcholine receptor signaling in tumor growth and metastasis.Journal of oncology · 2011Article
- Epigenetic effects and molecular mechanisms of tumorigenesis induced by cigarette smoke: an overview.Journal of oncology · 2011Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDA) is a lethal disease with etiological association with cigarette smoking. Nicotine, an important component of cigarettes, exists at high concentrations in the bloodstream of smokers. Osteopontin (OPN) is a secreted phosphoprotein that confers on cancer cells a migratory phenotype and activates signaling pathways that induce cell survival, proliferation, invasion, and metastasis. Here, we investigated the potential molecular basis of nicotine's role in PDA through studying its effect on OPN. Nicotine significantly (p < 0.02) increased OPN mRNA and protein secretion in PDA cells through activation of the OPN gene promoter. The OPN mRNA induction was inhibited by the nicotinic acetylcholine receptor antagonist, mechamylamine. Further, the tyrosine kinase inhibitor genistein inhibited the nicotine-mediated induction of OPN, suggesting that mitogen activated protein kinase signaling mechanism is involved. Nicotine activated the phosphorylation of ERK1/2, but not p38 or c-Jun NH2-terminal MAP kinases. Inhibition of ERK1/2 activation reduced the nicotine-induced OPN synthesis. Rats exposed to cigarette smoke showed a dose-dependent increase in pancreatic OPN that paralleled the rise of pancreatic and plasma nicotine levels. Analysis of cancer tissue from invasive PDA patients, the majority of whom were smokers, showed the presence of significant amounts of OPN in the malignant ducts and the surrounding pancreatic acini. Our data suggest that nicotine may contribute to PDA pathogenesis through upregulation of OPN. They provide the first insight into a nicotine-initiated signal transduction pathway that regulates OPN as a possible tumorigenic mechanism in PDA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.