Gene name: | MYCN |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | HEL,K562 |
Gene ID: | 4613 |
Category: | protein coding |
Phenotype: | Erythroleukemia |
Experimental category: | HL |
PMID: | 29022893 |
Experiment: | SA-β-gal activity assay//Flow cytometry//FCM analysis//qRT-PCR//Knockdown |
Description: | Suppression of MYCN resulted in increased senescence-associated acidic β-gal staining. Cell cycle analysis showed an increased percentage of cells with G0/G1 phase and a decreased percentage of cells with S phase in the MYCN-knockdown cells. The results showed that depletion of MYCN elevated the P21 expression in HEL cells analysis showed that etoposide treatment resulted in an increase in P21 expression, and MYCN depletion enhanced the etoposide-induced P21 activation in HEL cells. Further comparison analysis showed that overexpression of MYCN inhibited etoposide-mediated P21 activation in HEL and K562 cells. |
Target gene: | EZH2//P21 |
Official symbol(s): | EZH2//P21 |
R-AG-Target gene: | Upregulation//Downregulation |
Subcategory: | Unclear |
Target gene experiment: | qPCR//CHIP//Knockdown |
Target gene description: | The qPCR analysis showed that knockdown of MYCN significantly decreased the expression of EZH2 mRNA . The results showed that knockdown of MYCN led to significantly reduced enrichment of DNA binding in the EZH2 promoter. Further qPCR analysis showed that the expression of MYCN had positive correlation with the expression of EZH2 in the patients with acute erythroleukemia. The results showed that depletion of MYCN elevated the P21 expression in HEL cells. In this study, FCM analysis showed that etoposide treatment resulted in an increase in P21 expression, and MYCN depletion enhanced the etoposide-induced P21 activation in HEL cells . Further comparison analysis showed that overexpression of MYCN inhibited etoposide-mediated P21 activation in HEL and K562 cells. |
Regulatory pathway: | -- |
R-AG-Pathway: | -- |
Pathway experiment: | -- |
Pathway description: | -- |
Annotation:
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