| Gene name: | HMGB1 |
| Aging type: | Prevent |
| Aging characteristic: | Others |
| Tissue type: | Melanoma |
| Cell name: | A375,G361 |
| Experiment: | Knockdown//SA-β-gal activity assay//Flow cytometry//Cell proliferation assay |
| Description: | Knockdown of HMGB1 expression resulted in a marked reduction of cell proliferation and importantly, this effect appeared to be nicely correlated with the level of HMGB1 expression.Relative to the control cells, HMGB1- deficient cells showed a significant delay in cell cycle progression.We noticed that the HMGB1 stable knockdown cells appeared to be flatter in shape and larger in size than the matched control cells.This morphology change prompted us to ask whether HMGB1 depletion might induce cellular senescence. Measurement of senescent-associated β-galactosidase activity showed a marked increase of β-Gal-positive cells. |
| Target gene: | P21 |
| Official symbol(s): | P21 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Knockdown//SA-β-gal activity assay//Flow cytometry |
| Target gene description: | The result indicates that depletion of p21 expression almost completely abrogated G1 cell cycle arrest induced by HMGB1 deficiency.In addition,knockdown of p21 expression also abolished the senescent phenotype in HMGB1 deficient cells. |
| Regulatory pathway: | SP1 |
| R-AG-Pathway: | -- |
| Official symbol(s): | SP1 |
| Pathway experiment: | Luciferase reporter assay |
| Pathway description: | Consistent with a Sp1-dependent and p53-independent mechanism of p21 regulation, mutation of Sp1 but not p53 binding sites abrogated p21 induction by HMGB1-deficience. Almost identical results were obtained in both A375 and SK-MEL-28 cell lines. These data together confirm a Sp1-depdent mechanism of p21 induction by HMGB1-depletion. |
Annotation:
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