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

Michael B. Ujiki, Xian Zhong Ding, M. Reza Salabat, David J. Bentrem, Laleh Golkar, Ben Milam, Mark S. Talamonti, Richard H. Bell, Takeshi Iwamura, Thomas E. Adrian*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

158 Scopus citations


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.

Original languageEnglish (US)
Article number76
JournalMolecular Cancer
StatePublished - 2006

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Cancer Research


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