title: Apigenin inhibits pancreatic cancer cell proliferation through G2/M cell cycle arrest.
abstract: BACKGROUND
  Many chemotherapeutic agents have been used to treat pancreatic cancer without success. Apigenin, a naturally occurring flavonoid, has been shown to inhibit growth in some cancer cell lines but has not been studied in pancreatic cancer. We hypothesized that apigenin would inhibit pancreatic cancer cell growth in vitro.
  
  
  RESULTS
  Apigenin caused both time- and concentration-dependent inhibition of DNA synthesis and cell proliferation in four pancreatic cancer cell lines. Apigenin induced G2/M phase cell cycle arrest. Apigenin reduced levels of cyclin A, cyclin B, phosphorylated forms of cdc2 and cdc25, which are all proteins required for G2/M transition.
  
  
  CONCLUSIONS
  Apigenin inhibits growth of pancreatic cancer cells through suppression of cyclin B-associated cdc2 activity and G2/M arrest, and may be a valuable drug for the treatment or prevention of pancreatic cancer.
authors.affiliation: Department of Surgery and Robert H, Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. mujiki@northwestern.edu <mujiki@northwestern.edu>
authors.forename: Michael B
authors.initials: MB
authors.lastname: Ujiki
authors.forename: Xian-Zhong
authors.initials: XZ
authors.lastname: Ding
authors.forename: M Reza
authors.initials: MR
authors.lastname: Salabat
authors.forename: David J
authors.initials: DJ
authors.lastname: Bentrem
authors.forename: Laleh
authors.initials: L
authors.lastname: Golkar
authors.forename: Ben
authors.initials: B
authors.lastname: Milam
authors.forename: Mark S
authors.initials: MS
authors.lastname: Talamonti
authors.forename: Richard H
authors.initials: RH
authors.lastname: Bell
authors.forename: Takeshi
authors.initials: T
authors.lastname: Iwamura
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Adrian
mesh_terms: D047310:Apigenin / Q000494:pharmacology*; D015153:Blotting, Western; D016203:CDC2 Protein Kinase / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects*; D018797:Cell Cycle Proteins / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D019925:Cyclin A / Q000378:metabolism; D019926:Cyclin B / Q000378:metabolism; D004273:DNA, Neoplasm / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D016195:G2 Phase / Q000187:drug effects*; D006801:Humans; D008938:Mitosis / Q000187:drug effects*; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D010766:Phosphorylation / Q000187:drug effects; D020687:cdc25 Phosphatases / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D019925:Cyclin A; D019926:Cyclin B; D004273:DNA, Neoplasm; D019384:Nucleic Acid Synthesis Inhibitors; D047310:Apigenin; D016203:CDC2 Protein Kinase; C517009:CDC25C protein, human; D020687:cdc25 Phosphatases