| Gene name: | MIR22 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | MCF-7,MDA-MB-231,SiHa |
| Experiment: | SA-β-gal activity assay//qPCR//Western blot |
| Description: | Introduction of miR-22 into cancer cells caused a senescence-like phenotype, as observed by the increased senescence-associated β-galactosidase (SA-β-gal) activity.Thus, miR-22–mediated downregulation of MDC1 expression is a common mechanism in aging cells and is utilized indiverse and widespread tissue types in mammals. |
| Target gene: | MDC1//AKT1 |
| Official symbol(s): | MDC1//AKT1 |
| R-AG-Target gene: | Downregulation//-- |
| Subcategory: | Unclear |
| Target gene experiment: | qPCR//Western blot//Luciferase repoter assay |
| Target gene description: | Using real-time quantitative PCR (qPCR), we found that MDC1 mRNA was reduced more than 50% when miR-22 was overexpressed,indicating that miR-22 posttranscriptionally downregulates MDC1, probably by promoting both mRNA decay and inhibiting translation.We found that inhibition of endogenous miR-22 led to an increase in MDC1 protein and mRNA in CA-Akt1–overexpressing cells. Moreover, CA-Akt1 significantly inhibited MDC1 30-UTR luciferase activity relative to control.Under these experimental conditions, CA-Akt1–induced decrease of luciferase activity was significantly attenuated when anti–miR-22 was introduced, suggesting that CA-Akt1 negatively regulates MDC1 via miR-22. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
Loading,please wait...