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

Michael B Ujiki1, Xian-Zhong Ding, M Reza Salabat

  • 1Department of Surgery and Robert H, Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. mujiki@northwestern.edu <mujiki@northwestern.edu>

Molecular Cancer
|January 2, 2007
PubMed
Abstract

Insights

Apigenin, a natural flavonoid, effectively inhibited pancreatic cancer cell growth and proliferation in laboratory studies. This compound may offer a new therapeutic strategy for pancreatic cancer treatment or prevention.

Area of Science:

  • Oncology
  • Natural Products Chemistry
  • Cell Biology

Background:

  • Pancreatic cancer remains challenging to treat with conventional chemotherapy.
  • Apigenin, a flavonoid, shows anti-cancer properties but its effect on pancreatic cancer is unknown.

Purpose of the Study:

  • To investigate the efficacy of apigenin in inhibiting pancreatic cancer cell growth in vitro.

Main Methods:

  • Treatment of four pancreatic cancer cell lines with varying concentrations of apigenin.
  • Assessment of DNA synthesis and cell proliferation.
  • Cell cycle analysis using flow cytometry.
  • Western blot analysis to detect key cell cycle regulatory proteins.

Main Results:

  • Apigenin demonstrated dose- and time-dependent inhibition of pancreatic cancer cell DNA synthesis and proliferation.
  • Apigenin treatment resulted in G2/M phase cell cycle arrest.
  • Key proteins involved in G2/M transition, including cyclin A, cyclin B, and phosphorylated cdc2/cdc25, were reduced by apigenin.

Conclusions:

  • Apigenin effectively inhibits pancreatic cancer cell growth by disrupting the cell cycle at the G2/M phase.
  • Suppression of cyclin B-associated cdc2 activity is a key mechanism of apigenin's action.
  • Apigenin shows potential as a therapeutic agent for pancreatic cancer treatment or prevention.

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