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[Diclofenac suppresses hepatoma cell proliferation and promotes cyclooxygenase-2 mRNA expression]
1College of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China. yxbyjs@fimmu.com
Objective:
To investigate the effects of cyclooxygenase inhibitor diclofenac on the proliferation and cyclooxygenase-2 (COX-2) mRNA expression of cultured hepatocellular carcinoma cell lines HepG2, Hep3B and human hepatocellular cell line QSG-7701.
Methods:
After exposure to diclofenac at various concentrations (10-200 micromol/L) for 24, 48 and 72 h, the cell proliferation was analyzed by Cell Counting Kit-8 (CCK-8) assay and mRNA expression determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).
Results:
Diclofenac exposure for 24, 48 and 72 h significantly inhibited HepG2 and Hep3B cell proliferation in a concentration-dependent manner, with inhibition rate of 40.47% and 54.49% after 48 h exposure to 50 micromol/L diclofenac and IC50 of 70.54 and 48.39 micromol/L, respectively. A much weaker antiproliferative effect on QSG-7701 cells was shown, with IC50 of 189.91 micromol/L after 48-hour exposure to diclofenac. RT-PCR detected COX-2 mRNA in HepG2 and Hep3B cells, but hardly in QSG-7701 cells. Treatment with diclofenac or 5-Fu resulted in elevated COX-2 mRNA expression both in HepG2 and Hep3B cells.
Conclusion:
Diclofenac can specifically inhibit the proliferation of COX-2-expressing HepG2 and Hep3B cells, and induce up-regulation of COX-2 mRNA expression, which indicates the important role of COX-2 in the proliferation of hepatoma cells.
Insights
The cyclooxygenase inhibitor diclofenac effectively reduced hepatocellular carcinoma cell growth, particularly in COX-2 expressing HepG2 and Hep3B cells. This suggests cyclooxygenase-2 (COX-2) plays a key role in hepatoma cell proliferation.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Context:
- Hepatocellular carcinoma (HCC) is a significant global health concern.
- Cyclooxygenase-2 (COX-2) is implicated in cancer development and progression.
- Targeting COX-2 is a potential therapeutic strategy for HCC.
Purpose:
- To evaluate the impact of diclofenac, a COX inhibitor, on HCC cell proliferation.
- To assess diclofenac's effect on cyclooxygenase-2 (COX-2) mRNA expression in HCC cell lines.
- To investigate the relationship between COX-2 expression and diclofenac's antiproliferative activity.
Summary:
- Diclofenac demonstrated significant, dose-dependent inhibition of HepG2 and Hep3B cell proliferation.
- A weaker antiproliferative effect was observed in the non-COX-2 expressing QSG-7701 cell line.
- Diclofenac treatment led to increased COX-2 mRNA expression in HepG2 and Hep3B cells, while QSG-7701 cells showed minimal COX-2 expression.
Impact:
- Diclofenac specifically inhibits proliferation in COX-2 expressing HCC cells.
- The findings highlight the crucial role of COX-2 in hepatoma cell proliferation.
- This research provides insights into the therapeutic potential of targeting COX-2 in HCC.
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