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[Sodium Aescinate Induced Apoptosis of BGC-823 and AGS Cells by Inhibiting JAK-1/STAT-1 Signaling Pathway]
Objective:
To investigate the mechanism of sodium aescinate on the apoptosis of gastric cancer BGC-823 cells and AGS cells.
Methods:
CCK-8 assay was used to detect the cell viability of cancer cells; cells morphological changes were observed by inverted microscope; changes in nuclear morphology were observed by fluorescence inverted microscope after DAPI staining; cells apoptosis rate was detected by flow cytometry; Western blotting was used to detected the phosphorylation of JAK-1 and STAT-1; laser confocal microscopy was used to observed the nuclear translocation of STAT-1.
Results:
Sodium aescinate inhibited cells proliferation in a concentration dependent manner, and changed the cells morphology and nuclear morphology, significantly up-regulated the apoptosis rate of gastric cancer BGC-823 cells and AGS cells, and down-regulated the phosphorylation of JAK-1, STAT-1 protein, inhibited the nuclear translocation of STAT-1.
Conclusion:
Sodium aescinate inhibit the proliferation and induce apoptosis in the gastric cancer BGC-823 cells and AGS cells, and this process can be implemented by inhibiting the JAK-1/STAT-1 signaling pathway.
Insights
Sodium aescinate inhibits gastric cancer cell proliferation and induces apoptosis by affecting cell morphology and nuclear changes. This occurs through the inhibition of the JAK-1/STAT-1 signaling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Gastric cancer remains a significant global health challenge.
- Understanding novel therapeutic mechanisms is crucial for effective treatment strategies.
Purpose of the Study:
- To elucidate the mechanism by which sodium aescinate induces apoptosis in gastric cancer cells.
- To investigate the role of the JAK-1/STAT-1 signaling pathway in sodium aescinate's anti-cancer effects.
Main Methods:
- Cell viability was assessed using CCK-8 assays.
- Apoptosis, cell morphology, and nuclear changes were evaluated via flow cytometry and DAPI staining.
- Western blotting and laser confocal microscopy were employed to analyze JAK-1/STAT-1 phosphorylation and nuclear translocation.
Main Results:
- Sodium aescinate demonstrated dose-dependent inhibition of gastric cancer cell proliferation.
- Significant induction of apoptosis and alterations in cell/nuclear morphology were observed.
- Downregulation of JAK-1 and STAT-1 phosphorylation and inhibition of STAT-1 nuclear translocation were noted.
Conclusions:
- Sodium aescinate effectively inhibits proliferation and induces apoptosis in gastric cancer cells (BGC-823 and AGS).
- The anti-cancer effects are mediated through the inhibition of the JAK-1/STAT-1 signaling pathway.
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