ArticleJournal of cellular and molecular medicine2026
Single-Cell Multiomics Reveals That OTUD7B Is a Central Driver of Epithelial Remodelling and the Immunosuppressive Microenvironment in Pancreatic Ductal Adenocarcinoma.
Article in Journal of cellular and molecular medicine, 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
5 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PAAD) is characterized by extreme malignancy and profound resistance to therapy, largely driven by a fibrotic and immunosuppressive tumour microenvironment (TME). The deubiquitinase OTU domain-containing protein 7B (OTUD7B) has been implicated in inflammatory and oncogenic signalling, but its role in PAAD and its TME remains unclear. This study integrated single-cell RNA-seq datasets from the GEO and bulk RNA-seq data from the TCGA to delineate the cellular ecosystem of PAAD, and employed cell-cell communication analysis, high-dimensional weighted gene coexpression network analysis (hdWGCNA), and nonnegative matrix factorization (NMF) to identify OTUD7B-associated modules and epithelial subpopulations, while assessing the survival and clinicopathologic correlations of OTUD7B in the TCGA-PAAD cohort. Quantitative proteomics of OTUD7B-knockout PAAD cells was performed and combined with GO/KEGG and GSEA to explore downstream pathways, and immune infiltration was inferred by deconvolution algorithms and validated by multiplex immunofluorescence staining of OTUD7B, CD4, and FOXP3. Single-cell RNA-seq revealed the expansion of epithelial cells, fibroblasts, and macrophages with dense ligand-receptor networks, alongside the depletion of effector T and NK cells, indicating a shift toward an immunosuppressive TME. hdWGCNA identified epithelial-ECM modules in which OTUD7B served as a hub gene, and NMF revealed an OTUD7B-high epithelial subset enriched in glycosylation-related metabolic programs and positioned at an early stage of the malignant trajectory. OTUD7B was significantly upregulated in PAAD and was associated with higher grade, lymph node metastasis, and advanced stage, and predicted poorer overall survival. Proteomic profiling of OTUD7B-deficient cells revealed broad remodelling of mitochondrial oxidative phosphorylation, ROS metabolism, and redox homeostasis. OTUD7B expression was positively correlated with M2 macrophage infiltration, immunomodulatory gene expression, and CD4
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.