Inhibitions of Protein Kinase C and Proto-oncogene Expressions in NIH 3T3 Cells by Apigenin
Journal
European Journal of Cancer
Journal Volume
32
Journal Issue
1
Pages
146-151
Date Issued
1996
Abstract
Apigenin, a low-toxic and non-mutagenic plant flavonoid, suppresses 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-mediated tumour promotion of mouse skin. TPA has the ability to activate protein kinase C (PKC) and induce proto-oncogene expression. Our study shows that apigenin inhibits PKC by competing with ATP, and exhibits an IC50 value of 10 ± 0.5 μM. Apigenin also reduces the level of TPA-stimulated phosphorylation of cellular proteins. Of the protein tyrosine kinases tested, the fibroblast growth factor (FGF) receptor was most strongly affected by apigenin (IC50 20 μM), and pp60v-src most weakly affected (IC50 > 200 μM). Treatment of NIH 3T3 cells with 100 ng/ml TPA and 10, 50 and 100 μM apigenin resulted in 50, 80 and 100% suppression of TPA-induced C-JUN expression, respectively. Treatment of TPA with 10 μM apigenin inhibited TPA-induced C-FOS expression. TPA-stimulated cell growth was suppressed by 25 μM apigenin. Our results provide some evidence for understanding apigenin's inhibitory effects of TPA-mediated tumour promotion.
Subjects
Apigenin; C-FOS; C-JUN; Protein kinase C; Protein tyrosine kinases; TPA
SDGs
Other Subjects
apigenin; fibroblast growth factor receptor; flavanoid; protein kinase c; animal cell; article; cancer inhibition; cell strain 3t3; controlled study; gene expression; mouse; nonhuman; oncogene c fos; oncogene c jun; priority journal; proto oncogene; 3T3 Cells; Animals; Blotting, Northern; Cell Division; Chamomile; Dose-Response Relationship, Drug; Flavonoids; Gene Expression; Mice; Oils, Volatile; Phosphorylation; Plants, Medicinal; Protein Kinase C; Proto-Oncogene Proteins c-fos; Proto-Oncogene Proteins c-jun; RNA, Messenger; Tetradecanoylphorbol Acetate
Type
journal article