Apigenin inhibits pancreatic cancer cell proliferation through G2/M cell cycle arrest

Mol Cancer. 2006 Dec 29:5:76. doi: 10.1186/1476-4598-5-76.

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.

Conclusion: 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.

MeSH terms

  • Apigenin / pharmacology*
  • Blotting, Western
  • CDC2 Protein Kinase / metabolism
  • Cell Cycle / drug effects*
  • Cell Cycle Proteins / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cyclin A / metabolism
  • Cyclin B / metabolism
  • DNA, Neoplasm / antagonists & inhibitors
  • DNA, Neoplasm / biosynthesis
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • G2 Phase / drug effects*
  • Humans
  • Mitosis / drug effects*
  • Nucleic Acid Synthesis Inhibitors / pharmacology
  • Phosphorylation / drug effects
  • cdc25 Phosphatases / metabolism

Substances

  • Cell Cycle Proteins
  • Cyclin A
  • Cyclin B
  • DNA, Neoplasm
  • Nucleic Acid Synthesis Inhibitors
  • Apigenin
  • CDC2 Protein Kinase
  • CDC25C protein, human
  • cdc25 Phosphatases