ArticleSurgery2010
Induction of monocyte chemoattractant protein-1 by nicotine in pancreatic ductal adenocarcinoma cells: role of osteopontin.
Article in Surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Regulatory Roles of Osteopontin in Production of Monocyte-Origin MCP-1.Cell transplantation · 2018Article
- Association between monocyte chemoattractant protein-1 and blood pressure in smokers.The Journal of international medical research · 2018Article
- Endogenous CHRNA7-ligand SLURP1 as a potential tumor suppressor and anti-nicotinic factor in pancreatic cancer.Oncotarget · 2018Article
- Leptin signaling and cancer chemoresistance: Perspectives.World journal of clinical oncology · 2017Article
- The Role of nAChR and Calcium Signaling in Pancreatic Cancer Initiation and Progression.Cancers · 2015Review
- Osteopontin (OPN) isoforms, diabetes, obesity, and cancer; what is one got to do with the other? A new role for OPN.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2015Article
- RAN GTPase and Osteopontin in Pancreatic Cancer.Pancreatic disorders & therapy · 2013Article
- Apurinic/apyrimidinic endonuclease-1 (APE-1) is overexpressed via the activation of NF-κB-p65 in MCP-1-positive esophageal squamous cell carcinoma tissue.Journal of clinical biochemistry and nutrition · 2013Article
- Depletion of plasmacytoid dendritic cells inhibits tumor growth and prevents bone metastasis of breast cancer cells.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Effects of tobacco smoking and nicotine on cancer treatment.Pharmacotherapy · 2012Review
- Interplay between smoking-induced genotoxicity and altered signaling in pancreatic carcinogenesis.Carcinogenesis · 2012Review
- 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
- Excess risk of temporomandibular disorder associated with cigarette smoking in young adults.The journal of pain · 2012Article
- Nicotinic acetylcholine receptor signaling in tumor growth and metastasis.Journal of oncology · 2011Article
- Osteopontin in pancreatic cancer: A systematic review.Medicine internationalArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCigarette smoke and nicotine are among the leading environmental risk factors for developing pancreatic ductal adenocarcinoma (PDA). We showed recently that nicotine induces osteopontin (OPN), a protein that plays critical roles in inflammation and tumor metastasis. We identified an OPN isoform, OPNc, that is selectively inducible by nicotine and highly expressed in PDA tissue from smokers. In this study, we explored the potential proinflammatory role of nicotine in PDA through studying its effect on the expression of monocyte chemoattractant protein (MCP)-1 and evaluated the role of OPN in mediating these effects.
methodsMCP-1 mRNA and protein in PDA cells treated with or without nicotine (3-300 nmol/L) or OPN (0.15-15 nmol/L) were analyzed by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Luciferase-labeled promoter studies evaluated the effects of nicotine and OPN on MCP-1 transcription. Intracellular and tissue colocalization of OPN and MCP-1 were examined by immunofluorescence and immunohistochemistry.
resultsNicotine treatment significantly increased MCP-1 expression in PDA cells. Interestingly, blocking OPN with siRNA or OPN antibody abolished these effects. Transient transfection of the OPNc gene in PDA cells or their treatment with recombinant OPN protein significantly (P < .05) increased MCP-1 mRNA and protein and induced its promoter activity. MCP-1 was found in 60% of invasive PDA lesions, of whom 66% were smokers. MCP-1 colocalized with OPN in PDA cells and in the malignant ducts, and correlated well with higher expression levels of OPN in the tissue from patients with invasive PDA.
conclusionOur data suggest that cigarette smoking and nicotine may contribute to PDA inflammation by inducing MCP-1 and provide a novel insight into a unique role for OPN in mediating these effects.
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