| Gene name: | BRD4 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | MKN28 |
| Gene ID: | 23476 |
| Category: | protein coding |
| Phenotype: | Gastric cancer |
| Experimental category: | L |
| PMID: | 29434197 |
| Experiment: | SA-β-gal activity assay//Knockdown//Western blot |
| Description: | Depletion of Brd4, but not Brd2 and Brd3, increased the number of SA-β-Gal-positive cells.In line with increased SA-β-Gal activity, the levels of p21 were enhanced in Brd4 knockdown cells. |
| Regulatory pathway: | E2F-MIR-106B-P21 |
| R-AG-Pathway: | -- |
| Official symbol(s): | E2F-CDKN1A |
| Pathway experiment: | RT-PCR//Luciferase reporter assay//CHIP//Western blot |
| Pathway description: | Depletion of Brd4 or treatment of MKN28 cells with JQ1 up-regulated p21 mRNA levels with 2 3 folds induction in Brd4 knockdown cells and less than 2 folds induction in JQ1-treated cells.Consistently, depletion of Brd4 also increased the activity of 3 -UTR of p21 reporter. In contrast, overexpression of BRD4 in MKN28 cells decreased the luciferase activity of p21 3 -UTR luci- ferase reporter. When miR- 106b-5p and miR-519d-3p mimics were transfected into MKN28 cells followed by JQ1 treatment, miR-106b-5p but not miR-519d-3p mimics reduced the JQ1-induced cellular levels of p21, indicating that miR-106b targets p21 mRNA in MKN28 cells. Treatment of MKN28 cells with HLM006474 efficiently inhibited the binding of BRD4 to the promoter of miR-106b-5p,suggesting that E2F regulates the recruitment of BRD4 to the promoter of miR-106b-5p. Importantly, HLM006474 also down-regulated the expression of MCM7 and the expression of miR-106b-5p. |
Annotation:
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