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MPS1 is involved in the HPV16-E7-mediated centrosomes amplification

BACKGROUND: It has been reported that the oncoprotein E7 from human papillomavirus type 16 (HPV16-E7) can induce the excessive synthesis of centrosomes through the increase in the expression of PLK4, which is a transcriptional target of E2F1. On the other hand, it has been reported that increasing M...

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Autores principales: Alfaro-Mora, Yair, Domínguez-Gómez, Guadalupe, Cáceres-Gutiérrez, Rodrigo E., Tolentino-García, Laura, Herrera, Luis A., Castro-Hernández, Clementina, Bermúdez-Cruz, Rosa María, Díaz-Chávez, José
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8567613/
https://www.ncbi.nlm.nih.gov/pubmed/34736484
http://dx.doi.org/10.1186/s13008-021-00074-9
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author Alfaro-Mora, Yair
Domínguez-Gómez, Guadalupe
Cáceres-Gutiérrez, Rodrigo E.
Tolentino-García, Laura
Herrera, Luis A.
Castro-Hernández, Clementina
Bermúdez-Cruz, Rosa María
Díaz-Chávez, José
author_facet Alfaro-Mora, Yair
Domínguez-Gómez, Guadalupe
Cáceres-Gutiérrez, Rodrigo E.
Tolentino-García, Laura
Herrera, Luis A.
Castro-Hernández, Clementina
Bermúdez-Cruz, Rosa María
Díaz-Chávez, José
author_sort Alfaro-Mora, Yair
collection PubMed
description BACKGROUND: It has been reported that the oncoprotein E7 from human papillomavirus type 16 (HPV16-E7) can induce the excessive synthesis of centrosomes through the increase in the expression of PLK4, which is a transcriptional target of E2F1. On the other hand, it has been reported that increasing MPS1 protein stability can also generate an excessive synthesis of centrosomes. In this work, we analyzed the possible role of MPS1 in the amplification of centrosomes mediated by HPV16-E7. RESULTS: Employing qRT-PCR, Western Blot, and Immunofluorescence techniques, we found that E7 induces an increase in the MPS1 transcript and protein levels in the U2OS cell line, as well as protein stabilization. Besides, we observed that inhibiting the expression of MPS1 in E7 protein-expressing cells leads to a significant reduction in the number of centrosomes. CONCLUSIONS: These results indicate that the presence of the MPS1 protein is necessary for E7 protein to increase the number of centrosomes, and possible implications are discussed. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13008-021-00074-9.
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spelling pubmed-85676132021-11-04 MPS1 is involved in the HPV16-E7-mediated centrosomes amplification Alfaro-Mora, Yair Domínguez-Gómez, Guadalupe Cáceres-Gutiérrez, Rodrigo E. Tolentino-García, Laura Herrera, Luis A. Castro-Hernández, Clementina Bermúdez-Cruz, Rosa María Díaz-Chávez, José Cell Div Research BACKGROUND: It has been reported that the oncoprotein E7 from human papillomavirus type 16 (HPV16-E7) can induce the excessive synthesis of centrosomes through the increase in the expression of PLK4, which is a transcriptional target of E2F1. On the other hand, it has been reported that increasing MPS1 protein stability can also generate an excessive synthesis of centrosomes. In this work, we analyzed the possible role of MPS1 in the amplification of centrosomes mediated by HPV16-E7. RESULTS: Employing qRT-PCR, Western Blot, and Immunofluorescence techniques, we found that E7 induces an increase in the MPS1 transcript and protein levels in the U2OS cell line, as well as protein stabilization. Besides, we observed that inhibiting the expression of MPS1 in E7 protein-expressing cells leads to a significant reduction in the number of centrosomes. CONCLUSIONS: These results indicate that the presence of the MPS1 protein is necessary for E7 protein to increase the number of centrosomes, and possible implications are discussed. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13008-021-00074-9. BioMed Central 2021-11-04 /pmc/articles/PMC8567613/ /pubmed/34736484 http://dx.doi.org/10.1186/s13008-021-00074-9 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Alfaro-Mora, Yair
Domínguez-Gómez, Guadalupe
Cáceres-Gutiérrez, Rodrigo E.
Tolentino-García, Laura
Herrera, Luis A.
Castro-Hernández, Clementina
Bermúdez-Cruz, Rosa María
Díaz-Chávez, José
MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
title MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
title_full MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
title_fullStr MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
title_full_unstemmed MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
title_short MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
title_sort mps1 is involved in the hpv16-e7-mediated centrosomes amplification
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8567613/
https://www.ncbi.nlm.nih.gov/pubmed/34736484
http://dx.doi.org/10.1186/s13008-021-00074-9
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