ArticleCellular oncology (Dordrecht, Netherlands)2026
ADAMDEC1-driven CCL2-CCR2-PD-1 axis in esophageal squamous cell carcinoma: a dual threat of O-GlcNAcylation and m
Article in Cellular oncology (Dordrecht, Netherlands), 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
4 authors.
Funding
Abstract
objectiveEsophageal squamous cell carcinoma (ESCA) constitutes a major global health burden, with immune evasion and therapeutic resistance posing significant challenges. This study aims to elucidate the molecular mechanisms underlying ESCA immune escape and resistance to neoadjuvant therapy, focusing on the role of ADAMDEC1 in regulating the tumor microenvironment (TME) and immune evasion.
methodsWe performed transcriptome sequencing on 14 ESCA tumor tissues and adjacent non-tumor tissues from patients with or without neoadjuvant paclitaxel plus camrelizumab (PC) treatment. Bioinformatics analysis, functional validation, and in vitro and in vivo experiments were conducted to explore the regulatory mechanisms of ADAMDEC1 in ESCA. Patient-derived organoids (PDOs) and xenograft mouse models were utilized to assess the therapeutic effects of ADAMDEC1 knockout.
resultsADAMDEC1 was found to be overexpressed in ESCA tumor tissues and positively correlated with M2 macrophage infiltration. ADAMDEC1 promotes M2 polarization of tumor-associated macrophages (TAMs) through the CCL2-CCR2-PD-1 signaling axis, facilitating immune evasion. Mechanistically, ADAMDEC1 stabilizes O-GlcNAc transferase (OGT) via protein-protein interaction, enhancing O-GlcNAc glycosylation of YTHDF1. This post-translational modification increases YTHDF1’s stability and translational efficiency of GLI2 mRNA, thereby activating the CCL2-CCR2-PD-1 axis. Additionally, FTO was identified as a key regulator of GLI2 expression by modulating m6A methylation levels on GLI2 mRNA in a YTHDF1-dependent manner.
conclusionOur study reveals a novel ADAMDEC1-OGT-YTHDF1-GLI2 regulatory axis governing ESCA immune evasion and therapeutic resistance. Targeting this axis may provide a theoretical foundation for developing personalized immunotherapies and improving clinical outcomes in ESCA patients.
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.