Yair Alfaro-Mora, Guadalupe Domínguez-Gómez, Rodrigo E Cáceres-Gutiérrez, Laura Tolentino-García, Luis A Herrera, Clementina Castro-Hernández, Rosa María Bermúdez-Cruz, José Díaz-Chávez
{"title":"MPS1参与hpv16 - e7介导的中心体扩增。","authors":"Yair Alfaro-Mora, Guadalupe Domínguez-Gómez, Rodrigo E Cáceres-Gutiérrez, Laura Tolentino-García, Luis A Herrera, Clementina Castro-Hernández, Rosa María Bermúdez-Cruz, José Díaz-Chávez","doi":"10.1186/s13008-021-00074-9","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"16 1","pages":"6"},"PeriodicalIF":2.8000,"publicationDate":"2021-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8567613/pdf/","citationCount":"1","resultStr":"{\"title\":\"MPS1 is involved in the HPV16-E7-mediated centrosomes amplification.\",\"authors\":\"Yair Alfaro-Mora, Guadalupe Domínguez-Gómez, Rodrigo E Cáceres-Gutiérrez, Laura Tolentino-García, Luis A Herrera, Clementina Castro-Hernández, Rosa María Bermúdez-Cruz, José Díaz-Chávez\",\"doi\":\"10.1186/s13008-021-00074-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>\",\"PeriodicalId\":49263,\"journal\":{\"name\":\"Cell Division\",\"volume\":\"16 1\",\"pages\":\"6\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2021-11-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8567613/pdf/\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Division\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1186/s13008-021-00074-9\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Division","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s13008-021-00074-9","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
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 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.
期刊介绍：
Cell Division is an open access, peer-reviewed journal that encompasses all the molecular aspects of cell cycle control and cancer, cell growth, proliferation, survival, differentiation, signalling, gene transcription, protein synthesis, genome integrity, chromosome stability, centrosome duplication, DNA damage and DNA repair.
Cell Division provides an online forum for the cell-cycle community that aims to publish articles on all exciting aspects of cell-cycle research and to bridge the gap between models of cell cycle regulation, development, and cancer biology. This forum is driven by specialized and timely research articles, reviews and commentaries focused on this fast moving field, providing an invaluable tool for cell-cycle biologists.
Cell Division publishes articles in areas which includes, but not limited to:
DNA replication, cell fate decisions, cell cycle & development
Cell proliferation, mitosis, spindle assembly checkpoint, ubiquitin mediated degradation
DNA damage & repair
Apoptosis & cell death
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
