ArticleJournal of Cancer2024
DOT1L promotes expression of CD44 through the Wnt/β-catenin signaling pathway in early gastric carcinoma.
Article in Journal of Cancer, 2024. 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
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- HIPK2 exhibits context dependent dualistic effects and combinatorial inhibition of HIPK2-NLK-MAPK11 axis manifests synergism against gastric cancer.Human cell · 2026Article
- Cancer signaling networks in tumor progression and drug resistance: Crosstalk, adaptive reprogramming and therapeutic targeting (Review).Oncology reports · 2026Review
- DOT1L as a Therapeutic Target: Insights into Epigenetic Regulation and Cancer Treatment.Biomolecules & therapeutics · 2025Review
- Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025Review
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To assess telomere silencing 1-like (DOTIL) gene expression within gastric cancer (GC) tissues as well as its function of promoting cancer stem cell (CSC)-mediated epithelial-mesenchymal switching, tissue samples from 8 patients each in 3 stages (normal, low-grade intraepithelial neoplasia (LGIN), as well as early gastric carcinoma (EGC)) were collected for whole-exome sequencing, which revealed differentially expressed genes (DEGs). The DEGs and their prognostic value were verified through TCGA and GTEx analyses. We also verified the role of DOT1L in EGC development. We collected samples from three patients each with LGIN and EGC for single-cell sequencing. We conducted single-cell transcriptomic analysis, DEG analysis, cell‒cell interaction analysis, and pseudotime analysis using R language. Sites and levels of DOT1L, CD44 and DOT1L expression were verified by IF. We found 703 deleterious mutation sites in the LGIN group and 389 deleterious mutation sites in the EGC group. The LGIN as well as EGC categories exhibited increased levels of DOT1L expression compared to the standard category (P<0.05) in TCGA and GTEx. DOT1L also correlated significantly with TMB (P=8.45E-06), MSI (P=0.001), and tumor proliferation index (P=7.17E-09) in the TCGA and GTEx datasets. In single cells, we found that DOT1L promotes CD44 expression via the Wnt/β-catenin signaling pathway and the development for stemness properties within GC. In addition, we found that DOT1L, CD44 and CTNNB1 colocalize and correlate positively. In conclusion, one important CSC regulator in GC, DOT1L may be crucial in coordinating the expression of genes specific to a certain lineage during MSC development.
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Registered trials
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