MPS1参与人乳头瘤病毒16型E7介导的中心体扩增。
MPS1 is involved in the HPV16-E7-mediated centrosomes amplification.
作者信息
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
机构信息
Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados (CINVESTAV-IPN), Mexico City, Mexico.
Unidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cancerología (INCan), Mexico City, Mexico.
出版信息
Cell Div. 2021 Nov 4;16(1):6. doi: 10.1186/s13008-021-00074-9.
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.
背景
据报道，人乳头瘤病毒16型（HPV16）的癌蛋白E7可通过增加E2F1的转录靶点PLK4的表达来诱导中心体的过度合成。另一方面，据报道，增加MPS1蛋白的稳定性也会导致中心体的过度合成。在这项研究中，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、蛋白质免疫印迹和免疫荧光技术，我们发现E7可诱导U2OS细胞系中MPS1转录本和蛋白质水平增加，以及蛋白质稳定。此外，我们观察到在表达E7蛋白的细胞中抑制MPS1的表达会导致中心体数量显著减少。
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，并讨论了其可能的影响。
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