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Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Cell-cycle arrest at G2/M and growth inhibition by apigenin in human colon carcinoma cell lines

W Wang1, L Heideman, C S Chung

  • 1Department of Food Science and Human Nutrition, Iowa State University, Ames, Iowa 50011-1061, USA.

Molecular Carcinogenesis
|July 20, 2000
PubMed

Insights

Apigenin, a dietary flavonoid, halts colon cancer cell growth by inducing a reversible G2/M cell cycle arrest. This effect is linked to reduced p34(cdc2) kinase activity and protein levels, suggesting differential efficacy against tumors.

Area of Science:

  • Oncology
  • Cell Biology
  • Nutritional Science

Background:

  • Apigenin, a common dietary flavonoid, exhibits anti-cancer properties, including cell cycle arrest and inhibition of skin tumorigenesis.
  • Colon carcinoma is a significant health concern, necessitating research into novel therapeutic agents.

Purpose of the Study:

  • To investigate the effects of apigenin on cell growth and the cell cycle in human colon carcinoma cell lines (SW480, HT-29, Caco-2).
  • To elucidate the molecular mechanisms underlying apigenin's action on colon cancer cells.

Main Methods:

  • Cell viability and protein content assays were performed following apigenin treatment.
  • DNA flow cytometry was used to analyze cell cycle distribution.
  • Immune complex kinase assays and Western blot analyses were conducted to assess protein activity and levels (p34(cdc2), cyclin B1).

Main Results:

  • Apigenin caused a dose-dependent reduction in colon carcinoma cell number and protein content.
  • Apigenin induced a reversible G2/M phase cell cycle arrest in all three cell lines.
  • Apigenin inhibited p34(cdc2) kinase activity and decreased p34(cdc2) and cyclin B1 protein levels.

Conclusions:

  • Apigenin inhibits colon carcinoma cell growth by inducing a reversible G2/M arrest, partly through the inhibition of p34(cdc2) kinase.
  • The differential induction of G2/M arrest suggests apigenin may have varying effectiveness against colon tumors with different genetic profiles.

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