Suppression of protein kinase C and nuclear oncogene expression as possible molecular mechanisms of cancer chemoprevention by apigenin and curcumin

Jen K. Lin, Yen Chou Chen, Ying Tang Huang, Shoei Y. Lin-Shiau

研究成果: 雜誌貢獻文章

155 引文 斯高帕斯(Scopus)

摘要

Apigenin, a less-toxic and non-mutagenic flavonoid, suppressed 12-0- tetradecanoyl-phorbol-13-acetate-(TPA)-mediated tumor promotion of mouse skin. TPA had the ability to activate protein kinase C (PKC) and induced nuclear proto-oncogene expression. Our study indicates that apigenin inhibited PKC by competing with adenosine triphosphate (ATP). Apigenin also reduced the level of TPA-stimulated phosphorylation of cellular proteins and inhibited TPA-induced c-jun and c-fos expression. Curcumin, a dietary pigment phytopolyphenol, is also a potent inhibitor of tumor promotion induced by TPA in mouse skin. When mouse fibroblast cells were treated with TPA alone, PKC translocated from the cytosolic fraction to the particulate fraction. Treatment with 15 or 20 μM curcumin for 15 min inhibited TPA-induced PKC activity in the particulate fraction by 26-60%. Curcumin also inhibited PKC activity in vitro by completing with phosphatidylserine. Curcumin (10 μM) suppressed the expression of c-jun in TPA-treated cells. Fifteen flavonoids were examined for their effects on morphological changes in soft agar and cellular growth in v-H-ras transformed NIH3T3 cells. The results demonstrated that only apigenin, kaempferol, and genistein exhibited the reverting effect on the transformed morphology of these cells. Based on these findings, it is suggested that the suppression of PKC activity and nuclear oncogene expression might contribute to the molecular mechanisms of inhibition of TPA- induced tumor promotion by apigenin and curcumin.

原文英語
頁(從 - 到)39-48
頁數10
期刊Journal of Cellular Biochemistry
67
發行號SUPPL. 28/29
DOIs
出版狀態已發佈 - 1997
對外發佈Yes

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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