| Gene name: | DNMT1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | UCB-MSC |
| Experiment: | SA-β-gal activity assay//MTT assay |
| Description: | DNMT inhibition by 5-AzaC treatment induced cellular senescence, as shown by SA β-gal staining , and decreased the cellular proliferation rate in a dose-dependent manner, as shown by an MTT assay. |
| Target gene: | P16//P21/WAF1//EZH2//BMI1//MIR200C//MIR-214 |
| Official symbol(s): | P16//P21/WAF1//EZH2//BMI1//MIR200C//MIR-214 |
| R-AG-Target gene: | --//--//--//--//--//-- |
| Subcategory: | Unclear |
| Target gene experiment: | SA-β-gal activity assay//qPCR//Western blot |
| Target gene description: | SA β-galactosidase activity and expression levels of p16INK4A and p21CIP1/WAF1 were increased at day 3 of 5-AzaC treatment, and prominent changes were observed after 5 days of treatment with 5- AzaC.After inhibition of DNMT by 5-AzaC treatment, we observed decreased EZH2 and BMI1 expression levels. Because the significant decrease of EZH2 and BMI1 occurs after 3 days of treatment with 5-AzaC, we investigated miRNA expression levels at 1, 3 and 7 days after treatment with 5-AzaC and found that both mature and precursor miRNAs were increased at the time points indicated. After overexpression of miR-200c and miR-214, MSCs underwent cellular senescence, as shown by SA β-gal staining, and BMI1 and EZH2, the respective targets of miR200c and miR-214 were decreased, as shown by real-time qPCR. In addition, inhibition of miR-214 using antisense oligonucleotide transfection increased EZH2 expression. Although inhibition of miR-200c did not yield consistent results, overexpression of both miRNAs decreased their respective target (BMI1 and EZH2) at the mRNA level, suggesting that overexpressed miRNA during cellular senescence regulates the expression levels of BMI1 and EZH2. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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