Integrative proteogenomic characterization of hepatocellular carcinoma across etiologies and stages

Charlotte K. Y. Ng, Eva Dazert, Tuyana Boldanova, Mairene Coto-Llerena, Sandro Nuciforo, Caner Ercan, Aleksei Suslov, Marie-Anne Meier, Thomas Bock, Alexander Schmidt, Sylvia Ketterer, Xueya Wang, Stefan Wieland, Matthias S. Matter, Marco Colombi, Salvatore Piscuoglio, Luigi M. Terracciano, Michael N. Hall and Markus H. Heim ()
Additional contact information
Charlotte K. Y. Ng: University Hospital Basel, University of Basel
Eva Dazert: University of Basel
Tuyana Boldanova: University Hospital Basel, University of Basel
Mairene Coto-Llerena: University Hospital Basel, University of Basel
Sandro Nuciforo: University Hospital Basel, University of Basel
Caner Ercan: University Hospital Basel, University of Basel
Aleksei Suslov: University Hospital Basel, University of Basel
Marie-Anne Meier: University Hospital Basel, University of Basel
Thomas Bock: University of Basel
Alexander Schmidt: University of Basel
Sylvia Ketterer: University Hospital Basel, University of Basel
Xueya Wang: University Hospital Basel, University of Basel
Stefan Wieland: University Hospital Basel, University of Basel
Matthias S. Matter: University Hospital Basel, University of Basel
Marco Colombi: University of Basel
Salvatore Piscuoglio: University Hospital Basel, University of Basel
Luigi M. Terracciano: University Hospital Basel, University of Basel
Michael N. Hall: University of Basel
Markus H. Heim: University Hospital Basel, University of Basel

Nature Communications, 2022, vol. 13, issue 1, 1-18

Abstract: Abstract Proteogenomic analyses of hepatocellular carcinomas (HCC) have focused on early-stage, HBV-associated HCCs. Here we present an integrated proteogenomic analysis of HCCs across clinical stages and etiologies. Pathways related to cell cycle, transcriptional and translational control, signaling transduction, and metabolism are dysregulated and differentially regulated on the genomic, transcriptomic, proteomic and phosphoproteomic levels. We describe candidate copy number-driven driver genes involved in epithelial-to-mesenchymal transition, the Wnt-β-catenin, AKT/mTOR and Notch pathways, cell cycle and DNA damage regulation. The targetable aurora kinase A and CDKs are upregulated. CTNNB1 and TP53 mutations are associated with altered protein phosphorylation related to actin filament organization and lipid metabolism, respectively. Integrative proteogenomic clusters show that HCC constitutes heterogeneous subgroups with distinct regulation of biological processes, metabolic reprogramming and kinase activation. Our study provides a comprehensive overview of the proteomic and phophoproteomic landscapes of HCCs, revealing the major pathways altered in the (phospho)proteome.

Date: 2022
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-29960-8

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DOI: 10.1038/s41467-022-29960-8

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