Choline and nicotine increase glioblastoma cell proliferation by binding and activating α7- and α9- containing nicotinic receptors
[Display omitted] •Choline compounds are highly increased in glioblastoma cells.•Choline is also an agonist of α7- and α9-containing nicotinic receptors.•Both choline and nicotine promote glioblastoma cell proliferation and survival.•These effects are blocked by specific nicotinic antagonists or α7-...
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Published in | Pharmacological research Vol. 163; p. 105336 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Ltd
01.01.2021
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Abstract | [Display omitted]
•Choline compounds are highly increased in glioblastoma cells.•Choline is also an agonist of α7- and α9-containing nicotinic receptors.•Both choline and nicotine promote glioblastoma cell proliferation and survival.•These effects are blocked by specific nicotinic antagonists or α7- and/or α9 siRNAs.•Nicotinic antagonists also decrease basal glioblastoma cell proliferation.
Glioblastomas (GBMs), the most frequent and aggressive human primary brain tumours, have altered cell metabolism, and one of the strongest indicators of malignancy is an increase in choline compounds. Choline is also a selective agonist of some neuronal nicotinic acetylcholine receptor (nAChR) subtypes.
As little is known concerning the expression of nAChR in glioblastoma cells, we analysed in U87MG human grade-IV astrocytoma cell line and GBM5 temozolomide-resistant glioblastoma cells selected from a cancer stem cell-enriched culture, molecularly, pharmacologically and functionally which nAChR subtypes are expressed and,whether choline and nicotine can affect GBM cell proliferation.
We found that U87MG and GBM5 cells express similar nAChR subtypes, and choline and nicotine increase their proliferation rate and activate the anti-apoptotic AKT and pro-proliferative ERK pathways. These effects are blocked by the presence of non-cell-permeable peptide antagonists selective for α7- and α9-containing nicotinic receptors. siRNA-mediated silencing of α7 or α9 subunit expression also selectively prevents the effects of nicotine and choline on GBM cell proliferation.
Our findings indicate that nicotine and choline activate the signalling pathways involved in the proliferation of GBM cells, and that these effects are mediated by α7 and α9-containing nAChRs. This suggests that these nicotinic receptors may contribute to the aggressive behaviour of this tumor and may indicate new therapeutic strategies against high-grade human brain tumours. |
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AbstractList | Glioblastomas (GBMs), the most frequent and aggressive human primary brain tumours, have altered cell metabolism, and one of the strongest indicators of malignancy is an increase in choline compounds. Choline is also a selective agonist of some neuronal nicotinic acetylcholine receptor (nAChR) subtypes. As little is known concerning the expression of nAChR in glioblastoma cells, we analysed in U87MG human grade-IV astrocytoma cell line and GBM5 temozolomide-resistant glioblastoma cells selected from a cancer stem cell-enriched culture, molecularly, pharmacologically and functionally which nAChR subtypes are expressed and,whether choline and nicotine can affect GBM cell proliferation. We found that U87MG and GBM5 cells express similar nAChR subtypes, and choline and nicotine increase their proliferation rate and activate the anti-apoptotic AKT and pro-proliferative ERK pathways. These effects are blocked by the presence of non-cell-permeable peptide antagonists selective for α7- and α9-containing nicotinic receptors. siRNA-mediated silencing of α7 or α9 subunit expression also selectively prevents the effects of nicotine and choline on GBM cell proliferation. Our findings indicate that nicotine and choline activate the signalling pathways involved in the proliferation of GBM cells, and that these effects are mediated by α7 and α9-containing nAChRs. This suggests that these nicotinic receptors may contribute to the aggressive behaviour of this tumor and may indicate new therapeutic strategies against high-grade human brain tumours. [Display omitted] •Choline compounds are highly increased in glioblastoma cells.•Choline is also an agonist of α7- and α9-containing nicotinic receptors.•Both choline and nicotine promote glioblastoma cell proliferation and survival.•These effects are blocked by specific nicotinic antagonists or α7- and/or α9 siRNAs.•Nicotinic antagonists also decrease basal glioblastoma cell proliferation. Glioblastomas (GBMs), the most frequent and aggressive human primary brain tumours, have altered cell metabolism, and one of the strongest indicators of malignancy is an increase in choline compounds. Choline is also a selective agonist of some neuronal nicotinic acetylcholine receptor (nAChR) subtypes. As little is known concerning the expression of nAChR in glioblastoma cells, we analysed in U87MG human grade-IV astrocytoma cell line and GBM5 temozolomide-resistant glioblastoma cells selected from a cancer stem cell-enriched culture, molecularly, pharmacologically and functionally which nAChR subtypes are expressed and,whether choline and nicotine can affect GBM cell proliferation. We found that U87MG and GBM5 cells express similar nAChR subtypes, and choline and nicotine increase their proliferation rate and activate the anti-apoptotic AKT and pro-proliferative ERK pathways. These effects are blocked by the presence of non-cell-permeable peptide antagonists selective for α7- and α9-containing nicotinic receptors. siRNA-mediated silencing of α7 or α9 subunit expression also selectively prevents the effects of nicotine and choline on GBM cell proliferation. Our findings indicate that nicotine and choline activate the signalling pathways involved in the proliferation of GBM cells, and that these effects are mediated by α7 and α9-containing nAChRs. This suggests that these nicotinic receptors may contribute to the aggressive behaviour of this tumor and may indicate new therapeutic strategies against high-grade human brain tumours. |
ArticleNumber | 105336 |
Author | Gordon, Thomas J. Pucci, Susanna Viani, Paola McIntosh, Michael Clementi, Francesco Di Lascio, Simona Benfante, Roberta Moretti, Milena Zoli, Michele Fasoli, Francesca Gotti, Cecilia Daga, Antonio |
Author_xml | – sequence: 1 givenname: Susanna surname: Pucci fullname: Pucci, Susanna organization: CNR, Institute of Neuroscience, Milan, Italy – sequence: 2 givenname: Francesca surname: Fasoli fullname: Fasoli, Francesca organization: CNR, Institute of Neuroscience, Milan, Italy – sequence: 3 givenname: Milena surname: Moretti fullname: Moretti, Milena organization: CNR, Institute of Neuroscience, Milan, Italy – sequence: 4 givenname: Roberta orcidid: 0000-0001-5396-5429 surname: Benfante fullname: Benfante, Roberta organization: CNR, Institute of Neuroscience, Milan, Italy – sequence: 5 givenname: Simona orcidid: 0000-0002-5971-1515 surname: Di Lascio fullname: Di Lascio, Simona organization: Department of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy – sequence: 6 givenname: Paola surname: Viani fullname: Viani, Paola organization: Department of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy – sequence: 7 givenname: Antonio surname: Daga fullname: Daga, Antonio organization: Cellular Oncology, IRCCS Ospedale Policlinico San Martino, Genova, Italy – sequence: 8 givenname: Thomas J. surname: Gordon fullname: Gordon, Thomas J. organization: Department of Biology, University of Utah, Salt Lake City, UT, USA – sequence: 9 givenname: Michael surname: McIntosh fullname: McIntosh, Michael organization: Department of Biology, University of Utah, Salt Lake City, UT, USA – sequence: 10 givenname: Michele surname: Zoli fullname: Zoli, Michele organization: Department of Biomedical, Metabolic and Neural Sciences, Center for Neuroscience and Neurotechnology (CfNN), University of Modena and Reggio Emilia, 41125 Modena, Italy – sequence: 11 givenname: Francesco surname: Clementi fullname: Clementi, Francesco organization: CNR, Institute of Neuroscience, Milan, Italy – sequence: 12 givenname: Cecilia orcidid: 0000-0001-5358-8643 surname: Gotti fullname: Gotti, Cecilia email: cecila.gotti@in.cnr.it organization: CNR, Institute of Neuroscience, Milan, Italy |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33276105$$D View this record in MEDLINE/PubMed |
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Keywords | Gene silencing AKT1 and ERK1/2 Glioblastoma cell lines Proliferation Neuronal nicotinic receptors |
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•Choline compounds are highly increased in glioblastoma cells.•Choline is also an agonist of α7- and α9-containing nicotinic receptors.•Both... Glioblastomas (GBMs), the most frequent and aggressive human primary brain tumours, have altered cell metabolism, and one of the strongest indicators of... |
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SubjectTerms | AKT1 and ERK1/2 Gene silencing Glioblastoma cell lines Neuronal nicotinic receptors Proliferation |
Title | Choline and nicotine increase glioblastoma cell proliferation by binding and activating α7- and α9- containing nicotinic receptors |
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