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Andrographolide inhibits hepatocellular carcinoma progression and programmed death ligand-1 expression by blocking
Hairong Fu1, Yunchuan Yuan1, Jiahua Tan2
1Basic Medical College of Chongqing Three Gorges Medical College, Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area, Chongqing City, China.
Indian Journal of Pharmacology
|August 12, 2026
Summary
Andrographolide (AD) inhibits hepatocellular carcinoma (HCC) growth and immune evasion by blocking STAT3 phosphorylation and downregulating PD-L1 expression. This natural compound offers potential for novel HCC therapies.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Hepatocellular carcinoma (HCC) is an aggressive cancer known for recurrence and immune evasion.
- Programmed death ligand-1 (PD-L1) aids cancer immune evasion by suppressing T-cell activity.
- Andrographolide (AD) possesses anti-inflammatory, antiviral, and immunomodulatory properties with demonstrated antitumor effects.
Purpose of the Study:
- To investigate the antitumor and immune-activating effects of Andrographolide (AD) in hepatocellular carcinoma (HCC).
- To elucidate the mechanism by which AD affects HCC progression and PD-L1 expression, focusing on STAT3 signaling.
Main Methods:
- Utilized subcutaneous HCC mouse models and in vitro cell experiments (Huh-7 cells).
- Assessed AD's impact on cell proliferation, apoptosis, cell cycle, and PD-L1 expression using CCK-8, colony formation, apoptosis assays, western blot, immunofluorescence, and flow cytometry.
- Investigated AD's binding to STAT3 via molecular docking and cellular thermal shift assay; STAT3 dependency was confirmed using recombinant interleukin-6 (rIL-6).
Main Results:
- AD significantly inhibited tumor growth and decreased PD-L1 expression in vivo, while enhancing T-cell infiltration.
- In vitro, AD inhibited proliferation, induced apoptosis, and downregulated PD-L1 by suppressing STAT3 phosphorylation.
- Recombinant IL-6 treatment reversed the antitumor effects of AD, confirming STAT3 dependency.
Conclusions:
- Andrographolide (AD) effectively inhibits HCC progression and PD-L1 expression through the blockade of STAT3 phosphorylation.
- These findings provide a strong theoretical basis for developing AD-based therapeutic strategies against HCC.
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