ArticleJournal of gastroenterology2026
Single-cell analysis reveals crosstalk between TREM1-positive myeloid cells and cancer-associated fibroblasts in colorectal cancer progression.
Article in Journal of gastroenterology, 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
16 authors.
Funding
Abstract
backgroundThe limited efficacy of immunotherapy in colorectal cancer (CRC) underscores the need to better define immunosuppressive mechanisms within the tumor microenvironment (TME). We applied single-cell RNA sequencing (scRNA-seq) to characterize stromal-immune interactions shaping the CRC TME.
methodsPaired tumor and adjacent normal mucosa samples from eight patients with CRC were analyzed by scRNA-seq. Integrated bioinformatic approaches, including trajectory inference, transcriptional regulon analysis, and cell-cell communication modeling, were used to define cellular differentiation and intercellular signaling. Key findings were validated using The Cancer Genome Atlas datasets, multiplex immunofluorescence staining, and in vitro functional assays.
resultsTrajectory analysis demonstrated a progressive increase in triggering receptor expressed on myeloid cells 1 (TREM1) expression during tumor-associated myeloid differentiation. TREM1-positive myeloid cells exhibited enriched M2-like signatures and were preferentially associated with consensus molecular subtype 4 tumors, characterized by stromal activation and poor clinical outcomes. Stromal profiling identified an α-smooth muscle actin (ACTA2)-positive population associated with CRC progression. Spatial analyses revealed close localization of TREM1-positive myeloid cells and ACTA2-positive cancer-associated fibroblasts (CAFs) in tumor tissues. Mechanistically, integrated bioinformatic analyses indicated that TREM1-positive myeloid cells engage CAFs primarily through secreted phosphoprotein 1 (SPP1) signaling, while CAFs reinforce immunosuppressive myeloid phenotypes via TGF-β-associated extracellular matrix pathways. Functional assays showed that TREM1 inhibition reduced SPP1 expression and attenuated M2 macrophage polarization.
conclusionsThese findings identify a bidirectional interaction between TREM1-positive myeloid cells and CAFs that contributes to a profibrotic and immunosuppressive CRC microenvironment, highlighting the TREM1-SPP1 axis as a pathway of potential translational relevance.
Indexed as
Identifiers
What Socratic 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 Socratic graph.