Integrative proteogenomic characterization of hepatocellular carcinoma across etiologies and stages
Open accessAbstract
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.
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In patients with HCC, high PROX1 expression is associated with increased survival.
“in patients with HCC, high PROX1 expression or chromosomal amplifications including PROX1 were both associated with increased survival25–32”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [29]
The Results section on molecular subtypes reports survival associations for HCC clusters, but does not link survival to PROX1 expression. Searches for PROX1 and for amplifications including PROX1 returned no passage addressing that association in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measuredIn patients with HCC, chromosomal amplifications including PROX1 are associated with increased survival.
“in patients with HCC, high PROX1 expression or chromosomal amplifications including PROX1 were both associated with increased survival25–32”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [29]
The Results section on copy-number alterations identifies recurrent amplifications and candidate driver genes, but does not identify PROX1. The molecular-subtypes Results section reports improved overall survival for certain clusters, without linking that outcome to amplifications involving PROX1. Searches for PROX1 and PROX1 amplification with survival found no passage supporting the attributed association. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Ng, C. K. Y., Dazert, E., Boldanova, T., Coto-Llerena, M., Nuciforo, S., Ercan, C., Suslov, A., Meier, M.-A., Bock, T., Schmidt, A., Ketterer, S., Wang, X., Wieland, S., Matter, M. S., Colombi, M., Piscuoglio, S., Terracciano, L. M., Hall, M. N., & Heim, M. H.
- Affiliations
- University of Bern (CH)
- University of Basel (CH)
- Humanitas University (IT)
- Corresponding author
- Heim, Markus H.
- ORCID
- Venue
- Nature Communications
- Published
- 2022-05-04
- Volume
- 13
- Issue
- 1
- Pages
- 2436-2436
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9068765
- OpenAlex
- W4225410183
- Cited by
- 165
- References
- 108
- Citations by year
- 2026: 28 · 2025: 47 · 2024: 43 · 2023: 37 · 2022: 10
- FWCI
- 5.97
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- edoc (University of Basel) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Bern Open Repository and Information System (University of Bern) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- edoc (University of Basel)
- Funders
- Universität Basel
- Universitätsspital Basel
- Eidgenössische Technische Hochschule Zürich
- Associazione Italiana per la Ricerca sul Cancro (IG 2019—ID, IG-2019)
- Swiss Cancer Research Foundation (KFS-4543-08-2018, KFS-4988-02-2020-R)
- FP7 Ideas: European Research Council (609883)
- Topics
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Physical Sciences › Chemistry › Spectroscopy › Advanced Proteomics Techniques and Applications
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- hepatocellular carcinoma, proteogenomics, phosphoproteomics, cancer etiology, tumor stage, epithelial-mesenchymal transition, Wnt/β-catenin signaling, Akt/mTOR signaling, Notch signaling, cell cycle regulation, DNA damage response, metabolic reprogramming, AURKA, cyclin-dependent kinases, CTNNB1 mutation, TP53 mutation, protein phosphorylation, tumor heterogeneity, driver genes
- MeSH terms
- Proteogenomics, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Mutation, Proteomics, beta Catenin
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