| External factors: | MLN4924 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Intrahepatic cholangiocarcinoma |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Cell morphological analysis//Western blot//PI staining |
| Description: | Our flow cytometry analysis of DNA content evidenced a prominent increase in G2-M population 24h after treatment in cholangiocarcinoma cells. The arrest was confirmed to persist after longer treatment periods (48 and 72 h). In line with the role as a G2-M regulator, sharp increases of cell cycle inhibitors p21, p27, WEE1 (a well defined CRL substrate and an inhibitor of G2-M phase transition), and obvious decrease of a hallmark of M phase, p-Histone H3 (p-H3, ser10), were observed in QBC939 and RBE cells.in RBE cells, MLN4924 triggered senescence as demonstrated by an enlarged and flattened cellular shape as well as the expression of senescence-associated β-galactosidase. |
| Target gene: | CRL |
| R-EF-Target gene: | Upregulation |
| Official symbol(s): | CRL |
| Target gene experiment: | Western blot |
| Target gene description: | MLN4924 induced the accumulation of CRL substrates. Four tumor tissues were randomly selected from each group and lysed for immunoblotting analysis as indicated. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: