Diclofenac suppresses hepatoma cell proliferation and promotes cyclooxygenase-2 mRNA expression / 南方医科大学学报
Journal of Southern Medical University
; (12): 814-817, 2006.
Article
in Zh
| WPRIM
| ID: wpr-282910
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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).</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>
Full text:
1
Index:
WPRIM
Main subject:
Pathology
/
Pharmacology
/
RNA, Messenger
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Gene Expression Regulation, Enzymologic
/
Diclofenac
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Cyclooxygenase Inhibitors
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Carcinoma, Hepatocellular
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Reverse Transcriptase Polymerase Chain Reaction
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Cell Line, Tumor
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Cell Proliferation
Limits:
Humans
Language:
Zh
Journal:
Journal of Southern Medical University
Year:
2006
Type:
Article