A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma

Abstract Cancers evolve not only through the acquisition and clonal transmission of somatic mutations but also by epigenetic mechanisms that modify cell phenotype. Here, we use histology-guided and spatial transcriptomics to characterize hepatoblastoma, a childhood liver cancer that exhibits signifi...

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Main Authors: Peng V. Wu, Matt Fish, Florette K. Hazard, Chunfang Zhu, Sujay Vennam, Hannah Walton, Dhananjay Wagh, John Coller, Joanna Przybyl, Maurizio Morri, Norma Neff, Robert B. West, Roel Nusse
Format: Article
Language:English
Published: Nature Portfolio 2024-11-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-024-53802-4
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author Peng V. Wu
Matt Fish
Florette K. Hazard
Chunfang Zhu
Sujay Vennam
Hannah Walton
Dhananjay Wagh
John Coller
Joanna Przybyl
Maurizio Morri
Norma Neff
Robert B. West
Roel Nusse
author_facet Peng V. Wu
Matt Fish
Florette K. Hazard
Chunfang Zhu
Sujay Vennam
Hannah Walton
Dhananjay Wagh
John Coller
Joanna Przybyl
Maurizio Morri
Norma Neff
Robert B. West
Roel Nusse
author_sort Peng V. Wu
collection DOAJ
description Abstract Cancers evolve not only through the acquisition and clonal transmission of somatic mutations but also by epigenetic mechanisms that modify cell phenotype. Here, we use histology-guided and spatial transcriptomics to characterize hepatoblastoma, a childhood liver cancer that exhibits significant histologic and proliferative heterogeneity despite clonal activating mutations in the Wnt/β-catenin pathway. Highly proliferative regions with embryonal histology show high expression of Wnt target genes, the embryonic biliary transcription factor SOX4, and striking focal expression of the growth factor FGF19. In patient-derived tumoroids with constitutive Wnt activation, FGF19 is a required growth signal for FGF19-negative cells. Indeed, some tumoroids contain subsets of cells that endogenously express FGF19, downstream of Wnt/β-catenin and SOX4. Thus, the embryonic biliary lineage program cooperates with stabilized nuclear β-catenin, inducing FGF19 as a paracrine growth signal that promotes tumor cell proliferation, together with active Wnt signaling. In this pediatric cancer presumed to originate from a multipotent hepatobiliary progenitor, lineage-driven heterogeneity results in a functional growth advantage, a non-genetic mechanism whereby developmental lineage programs influence tumor evolution.
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spelling doaj-art-2d94ec01e9d046b7b6d307f07deb9f1b2024-11-24T12:32:34ZengNature PortfolioNature Communications2041-17232024-11-0115111910.1038/s41467-024-53802-4A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastomaPeng V. Wu0Matt Fish1Florette K. Hazard2Chunfang Zhu3Sujay Vennam4Hannah Walton5Dhananjay Wagh6John Coller7Joanna Przybyl8Maurizio Morri9Norma Neff10Robert B. West11Roel Nusse12Howard Hughes Medical Institute, Stanford University School of MedicineHoward Hughes Medical Institute, Stanford University School of MedicineDepartment of Pathology, Stanford University School of MedicineDepartment of Pathology, Stanford University School of MedicineDepartment of Pathology, Stanford University School of MedicineHoward Hughes Medical Institute, Stanford University School of MedicineStanford Genomics, Stanford UniversityStanford Genomics, Stanford UniversityDepartment of Pathology, Stanford University School of MedicineChan Zuckerberg BiohubChan Zuckerberg BiohubDepartment of Pathology, Stanford University School of MedicineHoward Hughes Medical Institute, Stanford University School of MedicineAbstract Cancers evolve not only through the acquisition and clonal transmission of somatic mutations but also by epigenetic mechanisms that modify cell phenotype. Here, we use histology-guided and spatial transcriptomics to characterize hepatoblastoma, a childhood liver cancer that exhibits significant histologic and proliferative heterogeneity despite clonal activating mutations in the Wnt/β-catenin pathway. Highly proliferative regions with embryonal histology show high expression of Wnt target genes, the embryonic biliary transcription factor SOX4, and striking focal expression of the growth factor FGF19. In patient-derived tumoroids with constitutive Wnt activation, FGF19 is a required growth signal for FGF19-negative cells. Indeed, some tumoroids contain subsets of cells that endogenously express FGF19, downstream of Wnt/β-catenin and SOX4. Thus, the embryonic biliary lineage program cooperates with stabilized nuclear β-catenin, inducing FGF19 as a paracrine growth signal that promotes tumor cell proliferation, together with active Wnt signaling. In this pediatric cancer presumed to originate from a multipotent hepatobiliary progenitor, lineage-driven heterogeneity results in a functional growth advantage, a non-genetic mechanism whereby developmental lineage programs influence tumor evolution.https://doi.org/10.1038/s41467-024-53802-4
spellingShingle Peng V. Wu
Matt Fish
Florette K. Hazard
Chunfang Zhu
Sujay Vennam
Hannah Walton
Dhananjay Wagh
John Coller
Joanna Przybyl
Maurizio Morri
Norma Neff
Robert B. West
Roel Nusse
A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma
Nature Communications
title A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma
title_full A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma
title_fullStr A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma
title_full_unstemmed A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma
title_short A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma
title_sort developmental biliary lineage program cooperates with wnt activation to promote cell proliferation in hepatoblastoma
url https://doi.org/10.1038/s41467-024-53802-4
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