ArticleOncogenesis2022
Non-genetic stratification reveals epigenetic heterogeneity and identifies vulnerabilities of glycolysis addiction in lung adenocarcinoma subtype.
Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- STAT3 Inhibition Prevents Adaptive Resistance and Augments NK Cell Cytotoxicity to KRASCancer science · 2025Article
- Excessive MYC Orchestrates Macrophages induced Chromatin Remodeling to Sustain Micropapillary-Patterned Malignancy in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Impact of histopathological subtypes on invasive lung adenocarcinoma: from epidemiology to tumour microenvironment to therapeutic strategies.World journal of surgical oncology · 2025Review
- Precise Molecular Subtyping Reveals Heterogeneity of Lung Adenocarcinoma Based on DNA Methylation.Current medicinal chemistry · 2025Article
- Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia.Cancer research · 2024Article
- Pathogenic role of super-enhancers as potential therapeutic targets in lung cancer.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Lung adenocarcinoma (LUAD) exhibits high heterogeneity and is well known for its high genetic variation. Recently, the understanding of non-genetic variation provides a new perspective to study the heterogeneity of LUAD. Little is known about whether super-enhancers (SEs) may be primarily responsible for the inter-tumor heterogeneity of LUAD. We used super-enhancer RNA (seRNA) levels of a large-scale clinical well-annotated LUAD cohort to stratify patients into three clusters with different prognosis and other malignant characteristics. Mechanistically, estrogen-related receptor alpha (ERRα) in cluster 3-like cell lines acts as a cofactor of BRD4 to assist SE-promoter loops to activate glycolysis-related target gene expression, thereby promoting glycolysis and malignant progression, which confers a therapeutic vulnerability to glycolytic inhibitors. Our study identified three groups of patients according to seRNA levels, among which patients in cluster 3 have the worst prognosis and vulnerability of glycolysis dependency. We also proposed a 3-TF index model to stratify patients with glycolysis-addicted tumors according to tumor SE stratification.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.