ArticleGenome biology2021
A systematic dissection of the epigenomic heterogeneity of lung adenocarcinoma reveals two different subclasses with distinct prognosis and core regulatory networks.
Article in Genome biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 33 citations in OpenAlex.
- Diagnostic performance of [European journal of nuclear medicine and molecular imaging · 2026Article
- Multiomics assessment of lung adenocarcinoma subtypes defined through tumor purity-adjusted DNA methylation.Genome medicine · 2026Article
- Construction of a prognostic model for lung adenocarcinoma based on disulfidptosis-related lncRNAs.Translational cancer research · 2025Article
- Construction of a prognostic model for lung adenocarcinoma based on necroptosis genes and its exploration of the potential for tumor immunotherapy.Translational cancer research · 2025Article
- MOGAN for LUAD Subtype Classification by Integrating Three Omics Data Types.Cancer innovation · 2025Article
- Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.Cell death discovery · 2025Review
- EAP: A versatile cloud-based platform for efficient quantitative analysis of large-scale ChIP/ATAC-seq datasets.Computational and structural biotechnology journal · 2025Article
- Precise Molecular Subtyping Reveals Heterogeneity of Lung Adenocarcinoma Based on DNA Methylation.Current medicinal chemistry · 2025Article
- Cell of origin alters myeloid-mediated immunosuppression in lung adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- An exosomes-related lncRNA prognostic model correlates with the immune microenvironment and therapy response in lung adenocarcinoma.Clinical and experimental medicine · 2024Article
- Pathogenic role of super-enhancers as potential therapeutic targets in lung cancer.Frontiers in pharmacology · 2024Review
- Advances in diagnosis and prediction for aggression of pure solid T1 lung cancer.Precision clinical medicine · 2023Article
- Circ_0001715 accelerated lung adenocarcinoma process by the miR-1322/CANT1 axis.Diagnostic pathology · 2023Article
- Molecular signature to predict quality of life and survival with glioblastoma using Multiview omics model.PloS one · 2023Article
- Non-genetic stratification reveals epigenetic heterogeneity and identifies vulnerabilities of glycolysis addiction in lung adenocarcinoma subtype.Oncogenesis · 2022Article
- HyperChIP: identification of hypervariable signals across ChIP-seq or ATAC-seq samples.Genome biology · 2022Article
- Single-cell RNA sequencing reveals the cellular and molecular changes that contribute to the progression of lung adenocarcinoma.Frontiers in cell and developmental biology · 2022Article
- Characterization of Necroptosis-Related Molecular Subtypes and Therapeutic Response in Lung Adenocarcinoma.Frontiers in genetics · 2022Article
- A pan-cancer analysis reveals role of clusterin (Frontiers in genetics · 2022Article
- tsRNA-5001a promotes proliferation of lung adenocarcinoma cells and is associated with postoperative recurrence in lung adenocarcinoma patients.Translational lung cancer research · 2021Article
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Authors and funding
19 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung adenocarcinoma (LUAD) is a highly malignant and heterogeneous tumor that involves various oncogenic genetic alterations. Epigenetic processes play important roles in lung cancer development. However, the variation in enhancer and super-enhancer landscapes of LUAD patients remains largely unknown. To provide an in-depth understanding of the epigenomic heterogeneity of LUAD, we investigate the H3K27ac histone modification profiles of tumors and adjacent normal lung tissues from 42 LUAD patients and explore the role of epigenetic alterations in LUAD progression.
resultsA high intertumoral epigenetic heterogeneity is observed across the LUAD H3K27ac profiles. We quantitatively model the intertumoral variability of H3K27ac levels at proximal gene promoters and distal enhancers and propose a new epigenetic classification of LUAD patients. Our classification defines two LUAD subgroups which are highly related to histological subtypes. Group II patients have significantly worse prognosis than group I, which is further confirmed in the public TCGA-LUAD cohort. Differential RNA-seq analysis between group I and group II groups reveals that those genes upregulated in group II group tend to promote cell proliferation and induce cell de-differentiation. We construct the gene co-expression networks and identify group-specific core regulators. Most of these core regulators are linked with group-specific regulatory elements, such as super-enhancers. We further show that CLU is regulated by 3 group I-specific core regulators and works as a novel tumor suppressor in LUAD.
conclusionsOur study systematically characterizes the epigenetic alterations during LUAD progression and provides a new classification model that is helpful for predicting patient prognosis.
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