ArticleNature communications2023
Alternative promoters in CpG depleted regions are prevalently associated with epigenetic misregulation of liver cancer transcriptomes.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Investigating the role of CpG islands and DNA methylation at 3'UTRs in cancer.Life science alliance · 2026Article
- Metabolic disease variants rewire gene regulation through disruption of DNA G-quadruplex structures.Genome biology · 2026Article
- FOXM1 influences DNA methylation to augment TACC3 alternative splicing directed by KAT2A in hepatocellular carcinoma.Clinical and molecular hepatology · 2026Article
- Crosstalk BetweenCancers · 2026Review
- Systematic transcriptome analysis reveals the function of alternative promoters in hematopoietic lineages.Stem cell reports · 2026Article
- A systematic guide for identifying transcription factors that directly regulate the expression of a gene of interest.Genome research · 2026Review
- Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).Oncology reports · 2026Review
- Epigenomic, transcriptomic, and proteomic characterization of breast cancer cell line reference samples.Cell reports methods · 2026Article
- G-quadruplex structures as modulators of alternative promoter usage.NAR genomics and bioinformatics · 2025Article
- Alternative Promoters Drive Transcriptomic Reprogramming and Prognostic Stratification in TNBC.NPJ systems biology and applications · 2025Article
- Light-regulated dual-targeting of NUCLEAR CONTROL OF PEP ACTIVITY establishes photomorphogenesis via interorganellar communication.Plant physiology · 2025Article
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- A subset of Polycomb-targeted transcription factor genes become hypermethylated yet upregulated in colorectal cancer.Computational and structural biotechnology journal · 2025Article
- Molecular Insights into Phytochemicals Mediated Epigenetic Regulation in Preclinical Models of Breast Cancer.Drug design, development and therapy · 2025Review
- Gene regulation by convergent promoters.Nature genetics · 2025Article
- Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application.Signal transduction and targeted therapy · 2024Review
- Comprehensive review and updated analysis of DNA methylation in hepatocellular carcinoma: From basic research to clinical application.Clinical and translational medicine · 2024Review
- Systematic perturbations of SETD2, NSD1, NSD2, NSD3, and ASH1L reveal their distinct contributions to H3K36 methylation.Genome biology · 2024Article
- G-quadruplex forming regions in GCK and TM6SF2 are targets for differential DNA methylation in metabolic disease and hepatocellular carcinoma patients.Scientific reports · 2024Article
- Pan-cancer transcriptome analysis reveals widespread regulation through alternative tandem transcription initiation.Science advances · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional regulation is commonly governed by alternative promoters. However, the regulatory architecture in alternative and reference promoters, and how they differ, remains elusive. In 100 CAGE-seq libraries from hepatocellular carcinoma patients, here we annotate 4083 alternative promoters in 2926 multi-promoter genes, which are largely undetected in normal livers. These genes are enriched in oncogenic processes and predominantly show association with overall survival. Alternative promoters are narrow nucleosome depleted regions, CpG island depleted, and enriched for tissue-specific transcription factors. Globally tumors lose DNA methylation. We show hierarchical retention of intragenic DNA methylation with CG-poor regions rapidly losing methylation, while CG-rich regions retain it, a process mediated by differential SETD2, H3K36me3, DNMT3B, and TET1 binding. This mechanism is validated in SETD2 knockdown cells and SETD2-mutated patients. Selective DNA methylation loss in CG-poor regions makes the chromatin accessible for alternative transcription. We show alternative promoters can control tumor transcriptomes and their regulatory architecture.
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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.