ArticleFrontiers in cell and developmental biology2020
ALKBH4 Functions as a Suppressor of Colorectal Cancer Metastasis via Competitively Binding to WDR5.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- ALKBH4 confers ferroptosis resistance and drives tumorigenesis via dysregulation of GPX4 in breast cancer cells.In vitro cellular & developmental biology. Animal · 2026Article
- Role of UGP2 as a Biomarker in Colorectal Cancer: Implications for Tumor Progression, Diagnosis, and Prognosis.Current issues in molecular biology · 2025Article
- Biological interpretation of DNA/RNA modification by ALKBH proteins and their role in human cancer.European journal of medical research · 2025Review
- ALKBH4 functions as a hypoxia-responsive tumor suppressor and inhibits metastasis and tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Dealkylation of Macromolecules by Eukaryotic α-Ketoglutarate-Dependent Dioxygenases from the AlkB-like Family.Current issues in molecular biology · 2024Review
- ALKBH4 impedes 5-FU Sensitivity through suppressing GSDME induced pyroptosis in gastric cancer.Cell death & disease · 2024Article
- Article
- WDR5 promotes the tumorigenesis of oral squamous cell carcinoma via CARM1/β-catenin axis.Odontology · 2022Article
- Bivalent Regulation and Related Mechanisms of H3K4/27/9me3 in Stem Cells.Stem cell reviews and reports · 2022Review
- ALKBH4 promotes tumourigenesis with a poor prognosis in non-small-cell lung cancer.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpithelial-Mesenchymal Transition (EMT) is a major process in the initiation of tumor metastasis, where cancer cells lose sessile epithelial potential and gain mesenchymal phenotype. Large-scale cell identity shifts are often orchestrated on an epigenetic level and the interplay between epigenetic factors and EMT progression was still largely unknown. In this study, we tried to identify candidate epigenetic factors that involved in EMT progression.
methodsColorectal cancer (CRC) cells were transfected with an arrayed shRNA library targeting 384 genes involved in epigenetic modification. Candidate genes were identified by real-time PCR. Western blot, RNA-seq and gene set enrichment analysis were conducted to confirm the suppressive role of ALKBH4 in EMT. The clinical relevance of ALKBH4 in CRC was investigated in two independent Renji Cohorts and a microarray dataset (GSE21510) from GEO database.
resultsWe screened for candidate epigenetic factors that affected EMT process and identified ALKBH4 as a candidate EMT suppressor gene, which was significantly downregulated in CRC patients. Decreased level of ALKBH4 was associated with metastasis and predicted poor prognosis of CRC patients. Follow-up functional experiments illustrated overexpression of ALKBH4 inhibited the invasion ability of CRC cells
conclusionsThis study illustrated that ALKBH4 may function as a novel metastasis suppressor of CRC, and inhibits H3K4me3 modification through binding WDR5 during EMT.
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