ArticleFunctional & integrative genomics2024
DNMT1/DNMT3a-mediated promoter hypermethylation and transcription activation of ICAM5 augments thyroid carcinoma progression.
Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- SNP-Driven LncRNA H19 dysregulation and CeRNA axis in breast and thyroid cancers among Pakistani females.Molecular biology reports · 2026Article
- N-acetyl Cysteine Reduces Behavioral Disorders of the First and Second-generation Weaned Mice through the Modulation of TAC and the DNMT1 Gene Expression in the Hippocampus.Current pharmaceutical design · 2026Article
- Integrative Multi-omics Analysis and Mendelian Randomization Reveal Potential Therapeutic Targets and their Stratification in Lung Squamous Cell Carcinoma.Current medicinal chemistry · 2026Article
- Plasma proteome-wide Mendelian randomization reveals multi-ancestry drug targets for gastric cancer.Frontiers in oncology · 2026Article
- Elevated ICAM5 as a promising predictor of poor prognosis in bladder cancer via EMT, immune microenvironment, and therapy resistance.PloS one · 2026Article
- Article
- Involvement ofJournal of inflammation research · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Promoter methylation is one of the most studied epigenetic modifications and it is highly relevant to the onset and progression of thyroid carcinoma (THCA). This study investigates the promoter methylation and expression pattern of intercellular adhesion molecule 5 (ICAM5) in THCA. CpG islands with aberrant methylation pattern in THCA, and the expression profiles of the corresponding genes in THCA, were analyzed using bioinformatics. ICAM5 was suggested to have a hypermethylation status, and it was highly expressed in THCA tissues and cells. Its overexpression promoted proliferation, mobility, and tumorigenic activity of THCA cells. As for the downstream signaling, ICAM5 was found to activate the MAPK/ERK and MAPK/JNK signaling pathways. Either inhibition of ERK or JNK blocked the oncogenic effects of ICAM5. DNA methyltransferases 1 (DNMT1) and DNMT3a were found to induce promoter hypermethylation of ICAM5 in THCA cells. Knockdown of DNMT1 or DNMT3a decreased the ICAM5 expression and suppressed malignant properties of THCA cells in vitro and in vivo, which were, however, restored by further artificial ICAM5 overexpression. Collectively, this study reveals that DNMT1 and DNMT3a mediates promoter hypermethylation and transcription activation of ICAM5 in THCA, which promotes malignant progression of THCA through the MAPK signaling pathway.
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