MPS1 is involved in the HPV16-E7-mediated centrosomes amplification
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Updated: Oct 14, 2025
In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
Published on: July 23, 2010
Yair Alfaro-Mora1,2, Guadalupe Domínguez-Gómez2, Rodrigo E Cáceres-Gutiérrez2
1Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados (CINVESTAV-IPN), Mexico City, Mexico.
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.
Insights
Human papillomavirus type 16 E7 protein (HPV16-E7) increases centrosome synthesis by stabilizing MPS1. Inhibiting MPS1 reduces centrosome amplification in E7-expressing cells, highlighting MPS1
Area of Science:
- Cell Biology
- Virology
- Cancer Research
Background:
- Human papillomavirus type 16 oncoprotein E7 (HPV16-E7) is known to induce excessive centrosome synthesis.
- HPV16-E7 achieves this by increasing PLK4 expression, a target of E2F1.
- Increased MPS1 protein stability is also linked to excessive centrosome synthesis.
Purpose of the Study:
- To investigate the role of MPS1 in HPV16-E7-mediated centrosome amplification.
- To determine if HPV16-E7 affects MPS1 transcript and protein levels or stability.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) to measure MPS1 transcript levels.
- Western Blotting to assess MPS1 protein levels and stability.
- Immunofluorescence microscopy to visualize and quantify centrosome numbers.
- Functional assays involving MPS1 inhibition in HPV16-E7 expressing cells.
Main Results:
- HPV16-E7 expression led to increased MPS1 transcript and protein levels in U2OS cells.
- HPV16-E7 also enhanced MPS1 protein stability.
- Inhibition of MPS1 expression significantly reduced centrosome numbers in E7-expressing cells.
Conclusions:
- MPS1 protein is essential for HPV16-E7 to induce centrosome number increase.
- These findings suggest MPS1 as a potential therapeutic target in HPV-related cancers.
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