Deciphering cholangiocarcinoma heterogeneity and specific progenitor cell niche of extrahepatic cholangiocarcinoma at single-cell resolution
Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtyp...
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| Published in | Journal of hematology and oncology Vol. 18; no. 1; pp. 66 - 19 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BioMed Central Ltd
23.06.2025
BioMed Central BMC |
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| Online Access | Get full text |
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| Abstract | Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches.
We performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models.
iCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D
cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D
progenitor niches.
We present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. |
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| AbstractList | Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches.BACKGROUNDCholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches.We performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models.METHODSWe performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models.iCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D+ progenitor niches.RESULTSiCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D+ progenitor niches.We present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs.CONCLUSIONWe present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. Abstract Background Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches. Methods We performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models. Results iCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D + cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D + progenitor niches. Conclusion We present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches. We performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models. iCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D progenitor niches. We present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. Background Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches. Methods We performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models. Results iCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D.sup.+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D.sup.+ progenitor niches. Conclusion We present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches. We performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models. iCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D.sup.+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D.sup.+ progenitor niches. We present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. BackgroundCholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches.MethodsWe performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models.ResultsiCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D+ progenitor niches.ConclusionWe present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs. |
| ArticleNumber | 66 |
| Audience | Academic |
| Author | Gu, Mingye Liu, Chunliang Zong, Yali Chen, Jianan Liu, Erdong Zhang, Yongjie Jiang, Youhai Liu, Yang Li, Jingfeng Meng, Zhengyuan Wang, Xiang Wang, Hongyang Tang, Jing Yu, Wenlong Fu, Jing |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40551145$$D View this record in MEDLINE/PubMed |
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Lab Invest doi: 10.1038/labinvest.3700285 |
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| Snippet | Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the... Background Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes.... BackgroundCholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling... Abstract Background Cholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes.... |
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| SubjectTerms | Analysis Animal models Animals B cells Bile Duct Neoplasms - genetics Bile Duct Neoplasms - pathology Bile ducts Biological response modifiers Cancer Cell cycle Cholangiocarcinoma Cholangiocarcinoma - genetics Cholangiocarcinoma - pathology Clinical trials DNA microarrays Drug resistance Epithelial cells Genes Genomes Genomics Humans Immunotherapy Inflammation Interferon Malignancy Medical prognosis Mice Microenvironments Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Oncology Organoids Patients Precision medicine Progenitor cells RNA RNA sequencing Senescence Single-Cell Analysis - methods Stem Cell Niche Stem cells Therapeutic targets Transcriptomics Tumor Microenvironment Tumorigenesis |
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| Title | Deciphering cholangiocarcinoma heterogeneity and specific progenitor cell niche of extrahepatic cholangiocarcinoma at single-cell resolution |
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