Aspirin inhibits the biological behavior of gallbladder carcinoma cells by modulating vascular endothelial growth factor
Related Experiment Video
Updated: Jul 6, 2025

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
Mingyuan Zhu1, Yanhua Huang1, Zhongcheng Zhou1
1Department of General Surgery, The Second Affiliated Hospital of Jiaxing University Jiaxing 314000, Zhejiang, China.
Objective:
To elucidate the effect of aspirin (ASP) on the biological behavior of gallbladder carcinoma (GBC) cells and its influence on vascular endothelial growth factor (VEGF) expression.
Methods:
Cell Counting Kit-8 (CCK-8) assay was performed to determine the effects of ASP on GBC-SD cell proliferation. In addition, Transwell assay and flow cytometry were carried out to observe the role of ASP in GBC-SD cell migration, invasion and apoptosis, respectively. Tumor necrosis factor-α (TNF-α), nuclear factor kappa-B (NF-κB), and VEGF concentrations in GBC-SD cells were examined by enzyme-linked immunosorbent assays (ELISAs).
Results:
ASP suppressed GBC-SD cell proliferation in a dose-dependent manner, and a concentration ≥ 2 mmol/L could significantly inhibit the migration and invasion of GBC-SD cells and induce apoptosis. In addition, the anticancer effect of ASP in GBC-SD cells may be linked to its inhibition of TNF-α, NF-κB, and VEGF levels.
Conclusions:
ASP may markedly inhibit GBC-SD cell growth by significantly reducing TNF-α, NF-κB and VEGF expression.
More Related Videos
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
GPCRs Regulate Adenylyl Cylase Activity
Mitogens and the Cell Cycle

