External factors
| External factors: |
Gypenoside L |
| Category: |
Chemical compounds |
| Experiment: |
SA-β-gal activity assay//qRT-PCR//EdU assay//Flow cytometry//Western blot |
| Description: |
Treatment with Gyp-L significantly increased the percentages of SA-β-gal-positive cells .The proportion of EdU-positive cells was higher in the control group, which was remarkably reduced in a concentration-dependent manner in the presence of Gyp-L, indicating that Gyp-L inhibited the proliferative activity of cancer cells.we detected the senescence-associated expression of SASP, such as IL-1α, IL-6, TIMP-1, CXCL-1 and CXCL-2, by qRT-PCR. As expected, the mRNA expression levels of all cytokines were increased by Gyp-L.Flow cytometry assay results demonstrated that a progressive increase of cells, retardant in S-phase, occurred in hepatic and esophagus cancer cells when treated with different concentrations of Gyp-L.Gyp-L significantly reduced the expression of all cell cycle regulators, such as CDK2, CDK4, CDK6, and cyclin D1, which was consistent with the arrested cell cycle. |
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Regulatory relationship
| Regulatory pathway:
|
MAPK//NF-κB//p38//ERK |
| R-EF-Pathway:
|
Activation//Activation//Activation//Activation |
| Official symbol(s): |
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MAPK//NFKB1//MAPK14//ERK
|
| Pathway experiment: |
Western blot |
| Pathway description: |
We found that Gyp-L activated MAPK signals, mainly through p38 and ERK signaling pathways, in a dose-dependent manner in esophageal cancer.To explore its potential regulation in Gyp-L-induced senescence, a western blotting experiment was performed, which showed that the phosphorylation and activation of NF-κB was markedly up-regulated by Gyp-L in ECA-109 cells.Gyp-L also activated p38 and ERK in a dose-dependent manner in HepG2 cells. |
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.