ArticleJournal of translational medicine2025
PPIF
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Cancer Heterogeneity and Cancer Cell Plasticity: Molecular Mechanisms and Precision Therapy.MedComm · 2026Review
- Neutrophil Heterogeneity: Molecules to Cellular Behavior.Life (Basel, Switzerland) · 2026Review
- Review
- Neutrophil extracellular traps: the hidden driver of gastrointestinal cancer and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Identification and experimental validation of mitochondria pathway related genes in acute myeloid leukemia.Frontiers in immunology · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo elucidate the mechanism through which tumor-associated neutrophil extracellular traps (NETs) contribute to the progression of colorectal cancer (CRC), characterize cellular populations within the CRC tumor microenvironment (TME), and identify potential therapeutic targets.
methodsWe retrieved the single-cell RNA-seq datasets of CRC from GEO, and performed clustering analysis and subgroup analysis on the quality-controlled single-cell transcriptome data. Subsequently, we interrogated signaling pathways, biological functions, developmental trajectories, survival outcomes, gene regulatory networks, and cellular communication among distinct cell subgroups to delineate tumor heterogeneity during CRC progression.
resultsOur analyses reveal that the DACH1+ and NKD1+ CRC subgroups play vital roles in the initiation, progression, and metastasis of CRC. PPIF+ neutrophil subgroups promote NETs formation and CRC progression by facilitating mitochondrial reactive oxygen species (mtROS) production. Meanwhile, the C1QC+ Mac, RACK1+ Tem, RACK1+ B, and RACK1+ Plasma subgroups exert certain immunosuppressive effects within CRC TME, thus promoting CRC progression. Moreover, RACK1 may serve as a key ecological niche gene in CRC. Furthermore, PPIF+ neutrophils modulate the TME via TNFSF14–TNFRSF14 and TNFSF14-LTBR checkpoint axes, thereby sustaining the CRC progression.
conclusionOur research findings have revealed the biological characteristics of CRC under the influence of NETs. Altogether, this study underlines the therapeutic potential value of targeting NETs-related mechanisms in the context of CRC.
Indexed as
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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.