ArticleCell death & disease2025
Endoplasmic reticulum stress-related super enhancer promotes epithelial-mesenchymal transformation in hepatocellular carcinoma through CREB5 mediated activation of TNC.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- Inhibition of PERK signaling suppresses tumor progression and blocks GP73-GRP78-dependent stromal activation in hepatocellular carcinoma.Neoplasia (New York, N.Y.) · 2026Article
- Tubulin autoregulation mediator TTC5 regulates neuronal morphology and migration.bioRxiv : the preprint server for biology · 2026Article
- ATF4 and CHOP coordinate endoplasmic reticulum stress-responsive gene programs through enhancer activation and chromatin looping.Nucleic acids research · 2026Article
- SNHG5 enhances colorectal cancer metastasis through RNA-protein interaction with GNB2 and activation of canonical Wnt signaling.Non-coding RNA research · 2026Article
- Circadian Dysregulation in Aging Alters Senescence and Inflammatory Pathways in a Sex- and Time-of-Day-Dependent Manner.bioRxiv : the preprint server for biology · 2026Article
- Targeting the miR-32533/CREB5 axis: a promising immunomodulatory and therapeutic strategy for Alzheimer's disease.Frontiers in immunology · 2026Article
- UNC93B1 promotes pancreatic cancer progression through modulation of cGAS-STING signaling.Frontiers in immunology · 2026Article
- Article
- KY216-tubulin complex captures VASH2 to inhibit NSCLC metastasis.Nature communications · 2025Article
- DPAGT1-Perspective as an Anticancer Drug Target.Molecules (Basel, Switzerland) · 2025Review
- Super-Enhancer DrivesAnimals : an open access journal from MDPI · 2025Article
- Endoplasmic reticulum stress sensor protein PERK in hepatic stellate cells promotes the progression of hepatocellular carcinoma via p38δ MAPK/IL-1β axis.Scientific reports · 2025Article
- Development and validation of a novel endoplasmic reticulum stress-related lncRNA signature in laryngeal squamous cell carcinoma.Scientific reports · 2025Article
- Targeting endoplasmic reticulum stress-induced CLGN resensitizes hepatocellular carcinoma to apoptosis: paeonol synergistically enhances efficacy by dual inhibition of CLGN and NF-κB.Frontiers in oncology · 2025Article
- Targeting super-enhancers in liver cancer: from pathogenic mechanisms to clinical applications.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Super-enhancers (SEs) are associated with key genes that control cellular state and cell identity. Endoplasmic reticulum stress (ERS) regulates epithelial-mesenchymal transformation (EMT). However, whether SEs are involved in ERS-related activation of EMT in hepatocellular carcinoma (HCC) is unknown. In this study, we identified 17 ERS-related SEs by comparing ERS-HCC cells with untreated control cells using ChIP-seq and RNA-seq. CRISPR-Cas9 and RT-qPCR identified CAMP responsive element binding protein 5 (CREB5) as a key target of ERS-related SE. Analyses of TCGA datasets and tissue arrays showed that CREB5 mRNA and protein expression levels were higher in liver cancer tissues than in paired normal tissues. In addition, overexpression of CREB5 was associated with poor prognosis and an aggressive phenotype in patients with HCC. We also found that activation of ERS enhanced the expression of CREB5, and upregulation of CREB5 significantly increased cell proliferation, migration, and invasion, and promoted EMT, but inhibited apoptosis. More importantly, ERS activation increased the expression of several EMT markers by modulating the expression of CREB5. Mechanistically, CREB5 upregulates the transcription of tenascin-C (TNC) by directly binding to its promoter region, thereby promoting EMT in liver cancer cells. In summary, our findings suggest that ERS activation promotes EMT in liver cancer cells via SE-mediated upregulation of the CREB5/TNC pathway. This result provides a new direction for uncovering how ERS regulates EMT and a foundation for preventing the progression of EMT in HCC.
Indexed as
Identifiers
What OpenQuestion holds
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.