ArticleThe Kaohsiung journal of medical sciences2023
DNMT3b affects colorectal cancer development by regulating FLI1 through DNA hypermethylation.
Article in The Kaohsiung journal of medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Dexmedetomidine Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting DNMT3B-Mediated Hypermethylation of the KLF4 Promoter.Cardiovascular drugs and therapy · 2026Article
- Unbiased profiling of translational landscape reveals TNFR2 as a translation-dependent vulnerability in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- A Swedish Haplotype GWAS in Familial and Sporadic Site-Specific Colorectal Cancer.International journal of molecular sciences · 2026Article
- DNMT3b promotes proliferation and invasion by mediating HOPX DNA methylation in lung cancer.iScience · 2026Article
- Carbonyl reductase 4 suppresses colorectal cancer progression through the DNMT3B/CBR4/FASN/mTOR axis.Cancer cell international · 2025Article
- DNA methylation-mediated suppression of TUSC1 expression regulates the malignant progression of esophagogastric junction cancer.Clinical epigenetics · 2024Article
- DNMT3b affects colorectal cancer development by regulating FLI1 through DNA hypermethylation.The Kaohsiung journal of medical sciences · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Friend leukemia integration 1 (FLI1) is an ETS transcription factor family member. Here, we identified cg11017065 as the most hyper-methylated cytosine and guanine (CpG) in colorectal cancer (CRC), which belongs to the FLI1 gene. Moreover, integrated bioinformatics prediction and analysis of our cohort showed that FLI1 expression was downregulated and DNA methylation was elevated in CRC. Bioinformatics prediction also indicated that patients overexpressing FLI1 had higher survival rates than those with low FLI1 expression. CRC cells with ectopic expression of FLI1 had reduced invasion, migration, cloning ability and increased apoptosis. Furthermore, DNA-methyltransferase 3b (DNMT3b) was found to be significantly overexpressed in CRC, and low DNMT3b expression predicted a prolonged survival. DNMT3b bound to the FLI1 promoter. Inhibition of DNMT3b increased FLI1 expression and inhibited the malignant phenotype of CRC cells. Inhibition of FLI1 reversed the phenotypic modulation by DNMT3b depletion in vitro and in vivo. In conclusion, our data indicate that DNMT3b potentiates CRC cell proliferation, migration, and invasion through downregulating FLI1.
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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.