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Curcumin reduces pulmonary tumorigenesis in vascular endothelial growth factor (VEGF)‐overexpressing transgenic mice
Author(s) -
Tung YuTang,
Chen HsiaoLing,
Lai ChengWei,
Shen ChihJie,
Lai YiWen,
Chen ChuanMu
Publication year - 2011
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201000654
Subject(s) - curcumin , cancer research , genetically modified mouse , angiogenesis , transgene , cyclin , vascular endothelial growth factor , carcinogenesis , cyclin d1 , cell cycle , cyclin d , cyclin a , biology , angiogenesis inhibitor , chemistry , pharmacology , cell , cancer , vegf receptors , biochemistry , gene , genetics
Scope: We investigated the inhibition of pulmonary tumor formation through treatment with curcumin in transgenic mice. Methods and results: In this study, a strain of transgenic mice carrying human vascular endothelial growth factor A 165 ( hVEGF‐A 165 ) gene to induce pulmonary tumor was used as an in vivo cancer therapy model. We found that curcumin significantly reduced hVEGF‐A 165 overexpression to normal, specifically in Clara cells of the lungs of transgenic mice, and suppressed the formation of tumors. In addition, we demonstrated a relationship between curcumin treatment and the expression of VEGF, EGFR, ERK2, and Cyclin A at the transcriptional and translational levels. We also noticed a reduction of Cyclin A and Cyclin B after curcumin treatment that had an effect on the cell cycle. Curcumin‐induced inhibition of Cyclin A and Cyclin B likely results in decreased progression through S and G2/M phases. These results demonstrated that the expression of proteins involved in the S to M phase transition in transgenic mice is suppressed by curcumin. Conclusion: A Data suggest that a blockade of the cell cycle may be a critical mechanism for the observed effects on vasculogenesis and angiogenesis following treatment with curcumin.