| External factors: | Dexamethasone |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Lung cancer |
| Experiment: | CCK-8 assay//SA-β-gal activity assay//Cell morphological analysis//SAHF |
| Description: | First, we noted that DDP caused remarkable and characteristic morphological alterations, including enlarged cellular size and a flattened shape in A549 cells and H292 cells, and DEX co-treatment attenuated these morphological alterations. DEX co-treatment also significantly affect the growth of A549 and H292 cell lines. DDP significantly induced increased SA-β-gal activity, and interestingly, DEX cotreatment decreased SA-β-gal activity compared with that of DDP treatment alone. DEX co-treatment could decrease the percentage of SAHFpositive cells compared with that of DDP treatment alone. |
| Regulatory pathway: | p53-p21 |
| R-EF-Pathway: | -- |
| Official symbol(s): | TP53-CDKN1A |
| Pathway experiment: | Western blot//qPCR//Luciferase reporter assay//SA-β-gal activity assay |
| Pathway description: | After DDP treatment, p53 protein gradually accumulated, and effect was strikingly weakened in the presence of DEX. The same trend was also detected about the protein expression of p21CIP1, a well-established transcriptional target and downstream effector of p53 with functions in cell cycle arrest, senescence induction and apoptosis . Similarly, p53 mRNA level was also increased after DDP treatment, and DEX co-treatment attenuated this increase. Furthermore, we also used luciferase reporter assays to detect p53 promoter activity, and the analysis showed DEX co-treatment could also attenuate p53 promoter activity compared with that of DDP treated group.After 2 days of DDP treatment with or without pcDNA3.1-/p53, we investigated that overexpression of p53 could prevent the decrease of SA-β-Gal activity in DEX co-treatment group. |
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