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Nicotine Induces the Up-regulation of the α7-Nicotinic Receptor (α7-nAChR) in Human Squamous Cell Lung Cancer Cells via the Sp1/GATA Protein Pathway.

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Title: Nicotine Induces the Up-regulation of the α7-Nicotinic Receptor (α7-nAChR) in Human Squamous Cell Lung Cancer Cells via the Sp1/GATA Protein Pathway.
Authors: Brown, Kathleen C.1, Perry, Haley E.1, Lau, Jamie K.1, Jones, Dennie V.2, Pulliam, Joseph F., Thornhill, Brent A.1, Crabtree, Clayton M.1, Haitao Luo3, Chen, Yi. Charlie3, Dasgupta, Piyali1 dasgupta@marshall.edu
Source: Journal of Biological Chemistry. 11/15/2013, Vol. 288 Issue 46, p33049-33059. 11p.
Subjects: Nicotine, Alkaloids, Nicotinic receptors, Cholinergic receptors, Squamous cell carcinoma
Abstract: Nicotine, the addictive component of cigarettes, promotes lung cancer proliferation via the α7-nicotinic acetylcholine receptor (α7-nAChR) subtype. The present manuscript explores the effect of nicotine exposure on α7-nAChR levels in squamous cell carcinoma of the lung (SCC-L) in vitro and in vivo. Nicotine (at concentrations present in the plasma of average smokers) increased α7-nAChR levels in human SCC-L cell lines. Nicotine-induced up-regulation of α7-nAChR was confirmed in vivo by chicken chorioallantoic membrane models. We also observed that the levels of α7-nAChR in human SCC-L tumors (isolated from patients who are active smokers) correlated with their smoking history. Nicotine increased the levels of α7-nAChR mRNA and α7-nAChR transcription in human SCC-L cell lines and SCC-L tumors. Nicotine-induced up-regulation of α7-nAChR required GATA4 and GATA6. ChIP assays showed that nicotine induced the binding of GATA4 or GATA6 to Sp1 on the α7-nAChR promoter, thereby inducing its transcription and increasing its levels in human SCC-L. Our data are clinically relevant because SCC-L patients smoked for decades before being diagnosed with cancer. It may be envisaged that continuous exposure to nicotine (in such SCC-L patients) causes up-regulation of α7-nAChRs, which facilitates tumor growth and progression. Our results will also be relevant to many SCC-L patients exposed to nicotine via second-hand smoke, electronic cigarettes, and patches or gums to quit smoking. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Biological Chemistry is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Nicotine Induces the Up-regulation of the α7-Nicotinic Receptor (α7-nAChR) in Human Squamous Cell Lung Cancer Cells via the Sp1/GATA Protein Pathway.
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  Data: <searchLink fieldCode="AR" term="%22Brown%2C+Kathleen+C%2E%22">Brown, Kathleen C.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Perry%2C+Haley+E%2E%22">Perry, Haley E.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Lau%2C+Jamie+K%2E%22">Lau, Jamie K.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Jones%2C+Dennie+V%2E%22">Jones, Dennie V.</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Pulliam%2C+Joseph+F%2E%22">Pulliam, Joseph F.</searchLink><br /><searchLink fieldCode="AR" term="%22Thornhill%2C+Brent+A%2E%22">Thornhill, Brent A.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Crabtree%2C+Clayton+M%2E%22">Crabtree, Clayton M.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Haitao+Luo%22">Haitao Luo</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Chen%2C+Yi%2E+Charlie%22">Chen, Yi. Charlie</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Dasgupta%2C+Piyali%22">Dasgupta, Piyali</searchLink><relatesTo>1</relatesTo><i> dasgupta@marshall.edu</i>
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Biological+Chemistry%22">Journal of Biological Chemistry</searchLink>. 11/15/2013, Vol. 288 Issue 46, p33049-33059. 11p.
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  Data: <searchLink fieldCode="DE" term="%22Nicotine%22">Nicotine</searchLink><br /><searchLink fieldCode="DE" term="%22Alkaloids%22">Alkaloids</searchLink><br /><searchLink fieldCode="DE" term="%22Nicotinic+receptors%22">Nicotinic receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Cholinergic+receptors%22">Cholinergic receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Squamous+cell+carcinoma%22">Squamous cell carcinoma</searchLink>
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  Data: Nicotine, the addictive component of cigarettes, promotes lung cancer proliferation via the α7-nicotinic acetylcholine receptor (α7-nAChR) subtype. The present manuscript explores the effect of nicotine exposure on α7-nAChR levels in squamous cell carcinoma of the lung (SCC-L) in vitro and in vivo. Nicotine (at concentrations present in the plasma of average smokers) increased α7-nAChR levels in human SCC-L cell lines. Nicotine-induced up-regulation of α7-nAChR was confirmed in vivo by chicken chorioallantoic membrane models. We also observed that the levels of α7-nAChR in human SCC-L tumors (isolated from patients who are active smokers) correlated with their smoking history. Nicotine increased the levels of α7-nAChR mRNA and α7-nAChR transcription in human SCC-L cell lines and SCC-L tumors. Nicotine-induced up-regulation of α7-nAChR required GATA4 and GATA6. ChIP assays showed that nicotine induced the binding of GATA4 or GATA6 to Sp1 on the α7-nAChR promoter, thereby inducing its transcription and increasing its levels in human SCC-L. Our data are clinically relevant because SCC-L patients smoked for decades before being diagnosed with cancer. It may be envisaged that continuous exposure to nicotine (in such SCC-L patients) causes up-regulation of α7-nAChRs, which facilitates tumor growth and progression. Our results will also be relevant to many SCC-L patients exposed to nicotine via second-hand smoke, electronic cigarettes, and patches or gums to quit smoking. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of Journal of Biological Chemistry is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1074/jbc.M113.501601
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        Text: English
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        StartPage: 33049
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      – SubjectFull: Nicotine
        Type: general
      – SubjectFull: Alkaloids
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      – SubjectFull: Nicotinic receptors
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      – SubjectFull: Cholinergic receptors
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      – SubjectFull: Squamous cell carcinoma
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      – TitleFull: Nicotine Induces the Up-regulation of the α7-Nicotinic Receptor (α7-nAChR) in Human Squamous Cell Lung Cancer Cells via the Sp1/GATA Protein Pathway.
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              Text: 11/15/2013
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