ArticleTranslational cancer research2019
DNA hypermethylation of the promoter attenuates forkhead box protein 3 (FOXP3) expression in hepatocellular carcinoma cells.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- Effects of Ionizing Radiation on DNA Methylation Patterns and Their Potential as Biomarkers.International journal of molecular sciences · 2025Review
- Cimetidine promotes STUB1-mediated degradation of tumoral FOXP3 by activating PI3K-Akt pathway in gastric cancer.Annals of translational medicine · 2020Article
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4 authors at 1 institution in 1 country.
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Abstract
backgroundForkhead box protein 3 (FOXP3) plays a pivotal role in tumor progression and impacts the methylation status and levels of expression of an associated promoter region. However, the methylation status and how this parameter impacts the FOXP3 promoter in cases of human hepatocellular carcinoma (HCC) remains unclear. This study sought to investigate the relationship between methylation status of transcriptional FOXP3 gene promoter and the levels of expression of FOXP3 in human HCC afflicted cell lines and tissues.
methodsWe used quantitative real-time PCR (Real-time qPCR) to detect the levels of expression of FOXP3 mRNA in human HCC afflicted cell lines and tissues. Immunohistochemistry and western blot were used to examine protein expression levels of FOXP3 in human HCC afflicted cell lines and tissues. Reverse transcription PCR was used to detect the levels of expression of the FOXP3 gene promoter in HCC afflicted cell lines. Finally, methylation sequencing was used to examine the influences of epigenetic regulation upon the FOXP3 promoter region in HCC afflicted cell lines.
resultsLevels of FOXP3 expression were down-regulated in HCC afflicted tissues compared with adjacent non-tumorous tissues. Levels of expression of FOXP3 in portal vein tumor thrombus (PVTT) were much lower than were levels in HCC afflicted tissues. Further, FOXP3 was abnormally expressed in HCC afflicted cell lines. The FOXP3 promoter was also abnormally expressed among HCC afflicted cell lines. Lastly, the FOXP3 promoter was hypermethylated in HCC afflicted cell lines.
conclusionsResults suggest that levels of expression of the FOXP3 promoter were decreased for measures of both mRNA and protein expression levels in HCC afflicted tissues and cell lines. The FOXP3 gene promoter region when hypermethylated may help inhibit FOXP3 expression and the development and progression of HCC.
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