title: Curcumin reduces pulmonary tumorigenesis in vascular endothelial growth factor (VEGF)-overexpressing transgenic mice.
abstract: METHODS
  We investigated the inhibition of pulmonary tumor formation through treatment with curcumin in transgenic mice.
  
  
  RESULTS
  In this study, a strain of transgenic mice carrying human vascular endothelial growth factor A₁₆₅ (hVEGF-A₁₆₅) gene to induce pulmonary tumor was used as an in vivo cancer therapy model. We found that curcumin significantly reduced hVEGF-A₁₆₅ 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
authors.forename: Yu-Tang
authors.initials: YT
authors.lastname: Tung
authors.forename: Hsiao-Ling
authors.initials: HL
authors.lastname: Chen
authors.forename: Cheng-Wei
authors.initials: CW
authors.lastname: Lai
authors.forename: Chih-Jie
authors.initials: CJ
authors.lastname: Shen
authors.forename: Yi-Wen
authors.initials: YW
authors.lastname: Lai
authors.forename: Chuan-Mu
authors.initials: CM
authors.lastname: Chen
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology; D003474:Curcumin / Q000494:pharmacology*; D019925:Cyclin A / Q000187:drug effects / Q000235:genetics; D019926:Cyclin B / Q000187:drug effects / Q000235:genetics; D004354:Drug Screening Assays, Antitumor; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D018773:Genes, erbB-1 / Q000187:drug effects; D005819:Genetic Markers / Q000187:drug effects; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D012333:RNA, Messenger; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics*
chemical_list: D019925:Cyclin A; D019926:Cyclin B; D005819:Genetic Markers; D012333:RNA, Messenger; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D003474:Curcumin