Abstract
BackgroundIt 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.ResultsEmploying 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.ConclusionsThese 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.
Highlights
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 transcrip‐ tional target of E2F1
Several studies have shown that the alteration of the function and/or stability of some proteins like CDK2-cyclin A/E complex [13,14,15], nucleophosmin chaperone (NPM1) [14], centrosomal protein CP110 [15], phosphatase CDC25B [16] and the kinases PLK4 [17] and MPS1 [18] promote an excessive synthesis of pre-existing centrioles
HPV16‐E7 increases MPS1 transcript and protein levels Because E7 deregulates proteins involved in the centrosome duplication cycle, such as PLK4 [35,36,37,38], MPS1 transcript and protein levels were determined due it is involved in centrosome duplication [18, 26,27,28]
Summary
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 transcrip‐ tional target of E2F1. It has been reported that increasing MPS1 protein stability can generate an excessive synthesis of centrosomes. Several studies have shown that the alteration of the function and/or stability of some proteins like CDK2-cyclin A/E complex [13,14,15], nucleophosmin chaperone (NPM1) [14], centrosomal protein CP110 [15], phosphatase CDC25B [16] and the kinases PLK4 [17] and MPS1 [18] promote an excessive synthesis of pre-existing centrioles.
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