ArticleIET systems biology
A Super-Enhancer-Related Ferroptosis Signature Predicts Survival and Immune Microenvironment in Colon Cancer Based on Bioinformatics Analyses and Experimental Validation.
Article in IET systems biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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.
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Who cites it
2 citing papers in PubMed.
- The DCBLD2 super-enhancer drives colorectal cancer progression through FOSL2/JUND-mediated activation of the CD146/AKT/TNFRSF6B pathway.Molecular biomedicine · 2026Article
- A Super-Enhancer-Related Ferroptosis Signature Predicts Survival and Immune Microenvironment in Colon Cancer Based on Bioinformatics Analyses and Experimental Validation.IET systems biologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Although immunotherapy has revolutionised cancer treatment, its benefits remain restricted to a minority of patients with colon cancer. Emerging evidence implicates super-enhancer (SE) networks and ferroptosis dysregulation as key oncogenic drivers, though their synergistic prognostic and immune microenvironment implications are unexplored. Super-enhancer-related ferroptosis genes (SEFGs) were identified by intersecting SE-associated and ferroptosis-related genes. Using TCGA-COAD (training) and GSE39582 (validation) cohorts, we established an 8-gene prognostic signature via LASSO Cox regression. This signature formed the basis of a clinical nomogram with robust calibration and discrimination (C-index = 0.813). High-risk patients exhibited significantly reduced overall survival. Elevated risk scores correlated with advanced stage, consensus molecular subtypes (CMS1/CMS4), high tumour mutation burden (TMB), high-level microsatellite instability (MSI) and enhanced immune cell infiltration, paradoxically coupled with immunosuppressive phenotypes including increased immune checkpoint gene expression and reduced immunotherapy responsiveness, alongside increased sensitivity to SE inhibitors. JQ-1 RNA-Seq profiling revealed three core SE-driven genes, TRIB2, CAV1 and ENO3, which were significantly downregulated upon SE inhibition. Among them, TRIB2 was distinguished by its SE recurrence, tumour overexpression, prognostic value and JQ-1 suppression. The SEFG signature facilitates simultaneous prediction of prognosis and assessment of the immune microenvironment, providing a potential tool for colon cancer management.
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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 Socratic graph.