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Differential apoptosis by gallotannin in human colon cancer cells with distinct p53 status

Sahar Al-Ayyoubi1, Hala Gali-Muhtasib

  • 1Department of Biology, The American University of Beirut, Beirut, Lebanon.

Molecular Carcinogenesis
|December 29, 2006
PubMed

Insights

Gallotannin (GT) inhibits colon cancer cell growth by arresting the cell cycle. It induces apoptosis in p53-deficient cells, revealing its chemopreventive potential through p53-independent mechanisms.

Area of Science:

  • Oncology
  • Molecular Biology
  • Natural Products Chemistry

Background:

  • Plant polyphenols, like Gallotannin (GT), exhibit anticarcinogenic properties.
  • Previous studies indicated GT's efficacy in preventing colon tumors in mice.
  • The precise molecular mechanisms underlying GT's chemopreventive effects remain largely unelucidated.

Purpose of the Study:

  • To investigate the molecular mechanisms of Gallotannin (GT) in colon cancer chemoprevention.
  • To determine GT's effects on human colon cancer cell lines with varying p53 statuses.
  • To identify potential molecular targets of GT in colon cancer therapy.

Main Methods:

  • Utilized isogenic HCT-116 colon cancer cell lines (p53+/+ and p53-/-) and normal intestinal cells (FHs 74Int).
  • Employed DNA flow cytometry to analyze cell-cycle progression and apoptosis.
  • Assessed protein and transcript levels of key cell-cycle regulators (p53, p21, cyclin D1, pRb) and apoptosis markers (Bax, Bcl-2).

Main Results:

  • GT inhibited the growth of HCT-116 cells and induced S-phase arrest in both p53+/+ and p53-/- lines.
  • In p53+/+ cells, GT increased p53 and p21 levels, decreased cyclin D1, pRb, and altered the Bax/Bcl-2 ratio, without inducing apoptosis.
  • GT induced significant apoptosis in p53-/- cells, marked by increased Bax/Bcl-2 ratios.

Conclusions:

  • Gallotannin (GT) inhibits colon cancer cell proliferation through p53-independent cell-cycle arrest.
  • GT demonstrates differential induction of apoptosis based on the p53 status of colon cancer cells.
  • These findings support GT's potential as a chemopreventive agent with distinct molecular actions.

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