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

IF 2.8 4区生物学 Q3 CELL BIOLOGY Cell Division Pub Date : 2021-11-04 DOI:10.1186/s13008-021-00074-9

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

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引用次数: 1

Abstract

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.

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MPS1参与hpv16 - e7介导的中心体扩增。

背景:据报道，来自人乳头瘤病毒16型(HPV16-E7)的癌蛋白E7可通过增加E2F1转录靶点PLK4的表达诱导中心体过度合成。另一方面，有报道称MPS1蛋白稳定性的增加也会导致中心体的过度合成。在这项工作中，我们分析了MPS1在HPV16-E7介导的中心体扩增中的可能作用。结果:采用qRT-PCR、Western Blot和免疫荧光技术，我们发现E7诱导U2OS细胞系MPS1转录物和蛋白水平升高，蛋白稳定。此外，我们观察到在E7蛋白表达的细胞中抑制MPS1的表达会导致中心体数量的显著减少。结论:这些结果表明MPS1蛋白的存在是E7蛋白增加中心体数量所必需的，并讨论了可能的影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Division CELL BIOLOGY-

CiteScore

3.70

自引率

0.00%

发文量

审稿时长

>12 weeks

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