ArticleBirth defects research2023
DNA methylation profile of lip tissue from congenital nonsyndromic cleft lip and palate patients by whole-genome bisulfite sequencing.
Article in Birth defects research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Genetic-epigenetic interactions (meQTLs) in orofacial clefts etiology.Molecular genetics and genomics : MGG · 2026Article
- Advancements in Pathogenic Genes and Biomarkers for Non-syndromic Cleft Lip With or Without Cleft Palate Via Multiomics.International dental journal · 2026Review
- The Evolution of Gene Sequencing Technologies: Unveiling Genetic Architecture of Nonsyndromic Orofacial Clefts.Genetics research · 2026Review
- Genetic-epigenetic interactions (meQTLs) in orofacial clefts etiology.medRxiv : the preprint server for health sciences · 2025Article
- DNA methylation profile of lip tissue from congenital nonsyndromic cleft lip and palate patients by whole-genome bisulfite sequencing.Birth defects research · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Congenital nonsyndromic cleft lip and palate (NSCLP) is one of the most common malformations worldwide. DNA methylation has been implicated in many diseases. However, its involvement in lip tissue from NSCLP is not well understood. This study aimed to investigate the role of dysregulated DNA methylation in NSCLP. DNA methylation profile was determined in eight injured and five self-normal lip tissue samples from children with NSCLP by whole-genome bisulfite sequencing. A total of 2,711 differentially methylated regions (DMRs), corresponding to 1,231 genes were identified. Given the important role of promoter methylation in regulating gene expression, the promoter DMR-related genes were considered. Bioinformatics analysis demonstrated that some of them showed potential associations with NSCLP. Therefore, the well-known NSCLP susceptibility gene, GLI family zinc finger 2 (GLI2) with an unknown role in its DNA methylation in NSCLP, was selected for further analysis. The promoter hypomethylation and higher mRNA expression level of GLI2 were observed in injured lip tissues by verification in additional samples. Moreover, dual luciferase reporter assay indicated that promoter hypermethylation of GLI2 inhibited its transcription. Overall, this study suggested that abnormal DNA methylation in lip tissue may be correlated with the pathogenesis of congenital NSCLP.
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