Nucleoporin Nup155 is part of the p53 network in liver cancer

Kerstin Holzer, Alessandro Ori, Amy Cooke, Daniel Dauch, Elisabeth Drucker, Philip Riemenschneider, Amparo Andres-Pons, Amanda L. DiGuilio, Marie-Therese Mackmull, Jochen Baßler, Stephanie Roessler, Kai Breuhahn, Lars Zender, Joseph S. Glavy, Frank Dombrowski, Ed Hurt, Peter Schirmacher, Martin Beck and Stephan Singer ()
Additional contact information
Kerstin Holzer: University Hospital Heidelberg
Alessandro Ori: Fritz-Lipmann-Institute (FLI)
Amy Cooke: Directors′ Research Unit
Daniel Dauch: University Hospital Tuebingen
Elisabeth Drucker: University Hospital Heidelberg
Philip Riemenschneider: University Medicine Greifswald
Amparo Andres-Pons: Structural and Computational Biology Unit
Amanda L. DiGuilio: Stevens Institute of Technology
Marie-Therese Mackmull: Structural and Computational Biology Unit
Jochen Baßler: Heidelberg University Biochemistry Center
Stephanie Roessler: University Hospital Heidelberg
Kai Breuhahn: University Hospital Heidelberg
Lars Zender: University Hospital Tuebingen
Joseph S. Glavy: Stevens Institute of Technology
Frank Dombrowski: University Medicine Greifswald
Ed Hurt: Heidelberg University Biochemistry Center
Peter Schirmacher: University Hospital Heidelberg
Martin Beck: Structural and Computational Biology Unit
Stephan Singer: University Hospital Heidelberg

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Cancer-relevant signalling pathways rely on bidirectional nucleocytoplasmic transport events through the nuclear pore complex (NPC). However, mechanisms by which individual NPC components (Nups) participate in the regulation of these pathways remain poorly understood. We discover by integrating large scale proteomics, polysome fractionation and a focused RNAi approach that Nup155 controls mRNA translation of p21 (CDKN1A), a key mediator of the p53 response. The underlying mechanism involves transcriptional regulation of the putative tRNA and rRNA methyltransferase FTSJ1 by Nup155. Furthermore, we observe that Nup155 and FTSJ1 are p53 repression targets and accordingly find a correlation between the p53 status, Nup155 and FTSJ1 expression in murine and human hepatocellular carcinoma. Our data suggest an unanticipated regulatory network linking translational control by and repression of a structural NPC component modulating the p53 pathway through its effectors.

Date: 2019
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DOI: 10.1038/s41467-019-10133-z

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