Promoter hypermethylation of let-7a-3 is relevant to its down-expression in diabetic nephropathy by targeting UHRF1

Profiling of circulating microRNAs in children with recent onset of type 1 diabetes

“…Let-7c-5p and let-7a-5p, 2 let-7 family members abundantly present in the serum, were negatively correlated with HbA1c levels in 2 separate cohorts. The promoter of let-7a-3 is reported to be hypermethylated in diabetic nephropathy, leading to its downregulation (35). Of all positively correlated miRNAs, 93% were present at low levels in the serum.…”

MEF2C mRNA expression and cognitive function in Japanese patients with Alzheimer's disease

“…Generally, an inverse relation is present between CpG methylation and transcriptional activity . In the promoter region, hypermethylation is usually related to transcriptional silencing . Although we selected target CpG sites that may theoretically bind major transcription factors in silico , an in vitro verification study, such as a luciferase‐reported assay, is needed to confirm that these target CpG sites are bound by transcription factors and regulate gene expression.…”

“…48,49 In the promoter region, hypermethylation is usually related to transcriptional silencing. 50,51 Although we selected target CpG sites that may theoretically bind major transcription factors in silico, an in vitro verification study, such as a luciferase-reported assay, is needed to confirm that these target CpG sites are bound by transcription factors and regulate gene expression. Other promoter regions or introns 21,22,52 may regulate MEF2C mRNA expression.…”

Mini-review: emerging roles of microRNAs in the pathophysiology of renal diseases

“…The let-7-TGF-␤1R1 connection illustrates another signal-amplifying loop involving miRNAs that can accelerate DN (65,66). Interestingly, the downregulation of let-7a-3 in DN was associated with promoter DNA hypermethylation, suggesting an epigenetic regulatory mechanism (114). TGF-␤1-induced decrease of miR130b was shown to upregulate its target, TGF-␤1R1, in MC through mechanisms involving a decrease in Ybx1/NFYC targeted by miR-216a, thus revealing another miRNA-mediated amplifying cascade (17).…”