ArticleBMC oral health2016
Krüppel-like factor 4 expression in oral carcinoma cells and hypermethylation at the gene promoter.
Article in BMC oral health, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 2 citations in OpenAlex.
- IGF2BP1-Mediates mActa Cardiologica Sinica · 2025Article
- Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer.BioMedicine · 2019Article
- Novel tumor-suppressor function of KLF4 in pediatric T-cell acute lymphoblastic leukemia.Experimental hematology · 2017Review
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Authors and funding
10 authors at 1 institution in 1 country.
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Abstract
backgroundKrüppel-like factor 4 (KLF4) is a transcription factor regulating proliferation-differentiation balance of epithelium, and down-regulated in less-differentiated and advanced oral carcinomas. Although the expression is inactivated by the promoter hypermethylation in malignant tumor cells, it remains unknown in oral carcinoma cells.
methodsGenomic DNA isolated from nine different oral carcinoma cell lines and a normal keratinocyte line was treated with sodium bisulfite, and methylation at KLF4 gene promoter was determined by PCR direct-sequence analysis. KLF4 expression in cells cultured with or without demethylation reagent was monitored by quantitative real-time PCR and immunoblot.
resultsA 237-bp promoter region spanning - 718 and - 482 of KLF4 gene was hypermethylated in oral carcinoma cells that express KLF4 at a low level, but the methylation was infrequent in cells expressing KLF4 high amount. The downstream region from - 481 to +192 was not methylated in any cell lines. Demethylation treatment of cells up-regulated the expression at mRNA and protein levels.
conclusionThis study demonstrated that hypermethylation at a narrow range of the promoter region down-regulates KLF4 expression, and suggests that the loss of expression by the hypermethylation contributes to oral carcinoma progression.
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