External factors
| External factors: |
MLN4924 |
| Category: |
Chemical compounds |
| Phenotype: |
Intrahepatic cholangiocarcinoma |
| Experimental category: |
HL |
| 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. |
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Regulatory relationship
| R-EF-Target gene:
|
Upregulation |
| 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. |
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Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
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