[Sodium Aescinate Induced Apoptosis of BGC-823 and AGS Cells by Inhibiting JAK-1/STAT-1 Signaling Pathway]

    Abstract

    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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