External factors: | Low-power laser irradiation |
Aging type: | Prevent |
Aging characteristic: |
Category: | Other |
Phenotype: | Aging |
Experiment: | SA-β-gal activity assay//Flow cytometry//Western blot |
Description: | Both overexpression of HA-FOXM1c and LPLI treatment alone inhibited UVB-induced cell senescence by SA-β-Gal staining assay. More importantly, overexpression of HA-FOXM1c with LPLI further suppressed the cell senescence.We found that LPLI inhibited the expression of p21 about 20% changes compared to UVBtreated cells at 24 h.The p21 expression decreased at 36 h was almost the same as control cells, ultimately inhibited UVB-induced cell senescence.We found that overexpression of HA-FOXM1c with/without LPLI treatment significantly decreased the percentage of cells at the G0/G1 phase, suggesting that the protective function was due to an indirect effect of a perturbation in cell cycle progression. |
Target gene: | P21 |
R-EF-Target gene: | Downregulation |
Official symbol(s): | P21 |
Target gene experiment: | Western blot//Knockdown |
Target gene description: | Overexpression of HA-FOXM1c promoted the expression of c-Myc with or without LPLI and inhibited the expression of p21, while adding PD98059 or knockdown of FOXM1 decreased c-Myc expression, and enhanced p21 expression even under LPLI. |
Regulatory pathway: | ERK-FOXM1 |
R-EF-Pathway: | Activation |
Official symbol(s): | ERK-FOXM1 |
Pathway experiment: | Western blot//RT-PCR |
Pathway description: | ERK translocation from cytoplasm to nucleus indicated that ERK was activated by LPLI, which was associated with phosphorylation as detected with Western blotting .Results show that LPLI increased the expression of FOXM1 at both protein and transcript levels, while PD98059 inhibited the effect of LPLI. |
Annotation: