ArticleTranslational oncology2026
MATR3 promotes proliferation and invasion of colon adenocarcinoma cells: bulk, single-cell transcriptomic analysis and experimental validation.
Article in Translational oncology, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMATR3 is a DNA/RNA binding nuclear matrix protein involved in RNA processing, transcriptional regulation, and DNA damage response. However, its role in colon adenocarcinoma (COAD) is still unclear.
methodsIntegrating transcriptomic data from TCGA-COAD and single-cell RNA sequencing data from GSE139555, evaluate the expression of MATR3 and its distribution in the tumor microenvironment. GeneMANIA, GO, KEGG, and GSEA analyses were used to explore the biological functions and pathways related to MATR3. The CIBERSORT and pRRophetic software packages are used to evaluate immune infiltration and drug sensitivity. The biological effects of MATR3 knockout were validated using qRT PCR, Western blotting, CCK-8, Transwell assays, and animal models.
resultsCompared with normal tissues, the expression of MATR3 was significantly upregulated in COAD tissues. Single cell analysis showed heterogeneity in the expression of MATR3 in tumor microenvironment cell populations, with relatively high expression in CD8+T cell subsets. Functional enrichment analysis showed that MATR3 related genes are mainly involved in RNA splicing, apoptosis related processes, mRNA monitoring, spliceosome pathways, and cell cycle regulation. The expression of MATR3 is associated with multiple immune cell populations and predicted drug responses. In vitro, MATR3 knockout inhibits the proliferation, migration, and invasion of HCT116 and Lovo cells. In vivo, the decrease in MATR3 expression inhibits tumor growth.
conclusionMATR3 is upregulated in COAD, which may promote tumor progression by regulating cell proliferation, invasion, cell cycle related pathways, and immune microenvironment. This study provides new insights into precision oncology.
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.