| Reciprocal effects of NNK and SLURP-1 on oncogene expression in target epithelial cells. | |
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MedLine Citation:
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PMID: 22369755 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS: To elucidate how the nicotinic acetylcholine receptors expressed on bronchial and oral epithelial cells targeted by the tobacco nitrosamine (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) (NNK) facilitate carcinogenic transformation. MAIN METHODS: Since NNK-dependent transformation can be abolished by the nicotinergic secreted mammalian Ly-6/urokinase plasminogen activator receptor related protein-1 (SLURP-1), we compared effects of NNK and recombinant (r)SLURP-1 on the expression of genes related to tumorigenesis in human immortalized bronchial and oral epithelial cell lines BEP2D and Het-1A, respectively. KEY FINDINGS: NNK stimulated expression of oncogenic genes, including MYB and PIK3CA in BEP2D, ETS1, NRAS and SRC in Het-1A, and AKT1, KIT and RB1 in both cell types, which could be abolished in the presence of rSLURP-1. Other cancer-related genes whose upregulation by NNK was abolishable by rSLURP-1 were the growth factors EGF in BEP2D cells and HGF in Het-1A cells, and the transcription factors CDKN2A and STAT3 (Het-1A only). NNK also upregulated the anti-apoptotic BCL2 (Het-1A) and downregulated the pro-apoptotic TNF (Het-1A), BAX and CASP8 (BEP2D), all of which could be abolished, in part, by rSLURP-1. NNK decreased expression of the CTNNB1 gene encoding the intercellular adhesion molecule β-catenin (BEP2D), as well as tumor suppressors CDKN3 and FOXD3 in BEP2D cells and SERPINB5 in Het-1A cells. These pro-oncogenic effects of NNK were abolished by rSLURP-1 that also upregulated RUNX3. SIGNIFICANCE: The obtained results identified target genes for both NNK and SLURP-1 and shed light on the molecular mechanism of their reciprocal effects on tumorigenic transformation of bronchial and oral epithelial cells. |
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Authors:
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Mina Kalantari-Dehaghi; Hans-Ulrich Bernard; Sergei A Grando |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-02-20 |
Journal Detail:
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Title: Life sciences Volume: 91 ISSN: 1879-0631 ISO Abbreviation: Life Sci. Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-11-12 Completed Date: 2013-01-24 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0375521 Medline TA: Life Sci Country: Netherlands |
Other Details:
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Languages: eng Pagination: 1122-5 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Dermatology, University of California, Irvine, CA 92697, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, Ly
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metabolism* Bronchi / cytology, drug effects, metabolism, pathology Carcinogens / metabolism Cell Line, Tumor Cell Transformation, Neoplastic / chemically induced*, genetics*, metabolism Epithelial Cells / drug effects, metabolism, pathology* Gene Expression Regulation, Neoplastic* / drug effects Humans Lung Neoplasms / chemically induced, genetics, metabolism, pathology Mouth / cytology, drug effects, metabolism, pathology Mouth Neoplasms / chemically induced, genetics, metabolism, pathology Nitrosamines / adverse effects*, metabolism Urokinase-Type Plasminogen Activator / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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DE14173/DE/NIDCR NIH HHS; ES017009/ES/NIEHS NIH HHS; R01 DE014173-01A1/DE/NIDCR NIH HHS; R01 ES017009/ES/NIEHS NIH HHS; R01 ES017009-01A2/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/ARS protein, human; 0/Antigens, Ly; 0/Carcinogens; 0/Nitrosamines; 64091-91-4/4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; EC 3.4.21.73/Urokinase-Type Plasminogen Activator |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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