ArticleTranslational oncology2026
Multi-omics interrogation identifies IRF4 as a causal transcription factor in monocytes that suppresses colorectal cancer progression by remodeling the immune microenvironment and inhibiting EMT.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough surgery and chemotherapy remain standard treatments for colorectal cancer (CRC), immunotherapy offers a promising avenue for patients with advanced disease. However, the cellular and molecular mechanisms underlying CRC progression and immune evasion are not fully elucidated.
methodsWe integrated single-cell RNA sequencing (GSE161277), bulk transcriptomic data (GEO and TCGA), and Mendelian randomization (MR) analysis to identify key cell subpopulations and transcription factors (TFs) causally associated with CRC. Spatial transcriptomics, multiple immune deconvolution algorithms, and in vitro experiments (including lentiviral-mediated IRF4 modulation, flow cytometry, and ELISA) were performed to validate the expression, immune regulatory function, and prognostic significance of the candidate TF.
resultsSingle-cell analysis identified monocytes as the most critical cell subpopulation in CRC pathogenesis. MR analysis revealed that IRF4, monocyte-associated TF, was causally linked to increased CRC risk. IRF4 expression was significantly downregulated in CRC tissues at both mRNA and protein levels, with elevated methylation and association with poor prognosis. Multi-omics immune profiling demonstrated that IRF4 correlated with immune cell infiltration, cancer immunity cycle scores, and immunotherapy response. Spatially, IRF4 was enriched in normal or low-malignant regions. Experimentally, IRF4 overexpression in HCT116 CRC cell enhanced CXCL8 and CCL5 secretion, increased the number of CD14
conclusionsIRF4, monocyte-associated TF, is a causal factor in CRC development. Its downregulation correlates with adverse prognosis and impaired antitumor immunity. IRF4 modulates the tumor microenvironment by regulating chemokine secretion, immune cell recruitment, and EMT, positioning it as a potential therapeutic target for CRC immunotherapy.
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.