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Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation
Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host c...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7549965/ https://www.ncbi.nlm.nih.gov/pubmed/32877289 http://dx.doi.org/10.1080/21505594.2020.1814091 |
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author | Dai, Xiaofeng Zhang, Xuanhao Miao, Yujie Han, Peiyu Zhang, Jianying |
author_facet | Dai, Xiaofeng Zhang, Xuanhao Miao, Yujie Han, Peiyu Zhang, Jianying |
author_sort | Dai, Xiaofeng |
collection | PubMed |
description | Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host cancer cells from undergoing cell lysis and foster them regain viability once the virotherapy was ceased. To explore CPV-induced cell cycle arrest and the underlying mechanism toward improved virotherapeutic design, we focus on epidermal growth factor receptor (EGFR), a cellular receptor interacting with TfR that mediates CPV-host interactions, and alterations on its tyrosine phosphorylation sites in response to CPV infection. We found that CPV could trigger host G1/S cell cycle arrest via the EGFR (Y1086)/p27 and EGFR (Y1068)/STAT3/cyclin D1 axes, and EGFR inhibitor could not reverse this process. Our results contribute to our understandings on the mechanism of CPV-induced host cellular response and can be used in the onco-therapeutic design utilizing CPV by preventing host cancer cells from entering cell cycle arrest. |
format | Online Article Text |
id | pubmed-7549965 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-75499652020-10-22 Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation Dai, Xiaofeng Zhang, Xuanhao Miao, Yujie Han, Peiyu Zhang, Jianying Virulence Research Paper Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host cancer cells from undergoing cell lysis and foster them regain viability once the virotherapy was ceased. To explore CPV-induced cell cycle arrest and the underlying mechanism toward improved virotherapeutic design, we focus on epidermal growth factor receptor (EGFR), a cellular receptor interacting with TfR that mediates CPV-host interactions, and alterations on its tyrosine phosphorylation sites in response to CPV infection. We found that CPV could trigger host G1/S cell cycle arrest via the EGFR (Y1086)/p27 and EGFR (Y1068)/STAT3/cyclin D1 axes, and EGFR inhibitor could not reverse this process. Our results contribute to our understandings on the mechanism of CPV-induced host cellular response and can be used in the onco-therapeutic design utilizing CPV by preventing host cancer cells from entering cell cycle arrest. Taylor & Francis 2020-09-02 /pmc/articles/PMC7549965/ /pubmed/32877289 http://dx.doi.org/10.1080/21505594.2020.1814091 Text en © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Dai, Xiaofeng Zhang, Xuanhao Miao, Yujie Han, Peiyu Zhang, Jianying Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation |
title | Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation |
title_full | Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation |
title_fullStr | Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation |
title_full_unstemmed | Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation |
title_short | Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation |
title_sort | canine parvovirus induces g1/s cell cycle arrest that involves egfr tyr1086 phosphorylation |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7549965/ https://www.ncbi.nlm.nih.gov/pubmed/32877289 http://dx.doi.org/10.1080/21505594.2020.1814091 |
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