ArticleFrontiers in cell and developmental biology2026
TRIM26 deficiency drives gastric cancer lymph node metastasis via TGF-β signaling activation and modulates gemcitabine response.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Integrating multiple omics and machine learning to reveal the prognostic value of endoplasmic reticulum stress geneTranslational cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Globally, gastric cancer (GC) is a predominant cause of cancer-related death. Lymph node metastasis (LNM) and chemoresistance constitute two major barriers to improving outcomes, as LNM signifies advanced disease and chemoresistance consequently leads to treatment failure. This study systematically investigates the key molecular drivers underlying LNM and chemoresistance in GC to assess their therapeutic relevance. Methods: Our study integrated single-cell and bulk transcriptomic data from GEO and TCGA. The analytical workflow comprised: Firstly, hdWGCNA for co-expression network construction; Secondly, a combination of machine learning algorithms (LASSO, random forest, and SVM-RFE) for core gene screening; Thirdly, pseudotime trajectory analysis (Monocle2/3) to delineate cell state transitions. Cell-cell communication and metabolic pathways were profiled using CellChat and scMetabolism, respectively. Computational pharmacology involved drug sensitivity prediction with the pRRophetic algorithm, complemented by molecular docking and dynamics simulations for structural insights. Finally, TRIM26's functional roles were experimentally validated through CCK-8, Transwell, and colony formation assays, alongside protein-level verification by immunohistochemistry. Results: Downregulation of TRIM26 in GC correlated strongly with LNM and poor survival. At single-cell resolution, TRIM26 loss in epithelial cells fueled pro-metastatic crosstalk with endothelial cells and macrophages through SELE-CD44 and SPP1-CD44/integrin axes. This triggered TGF-β activation, TP53 network dysregulation, and metabolic reprogramming of taurine and pantothenate/CoA pathways. TRIM26-low tumors were predicted to be less sensitive to gemcitabine, consistent with higher estimated IC Conclusion: TRIM26 inhibits LNM by modulating TGF-β signaling and remodeling the tumor microenvironment. Clinically, low TRIM26 expression identifies tumors with reduced sensitivity to gemcitabine, reflected by higher estimated IC
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.