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Silibinin triggers apoptosis and cell-cycle arrest of SGC7901 cells

Yuanxin Zhang1, Quanshun Li, Yakun Ge

  • 1Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, Jilin University, Changchun, 130012, China.

Phytotherapy Research : PTR
|May 24, 2012
PubMed

Insights

Silibinin, a flavonoid, inhibits gastric cancer cell growth by inducing cell-cycle arrest and apoptosis. This chemopreventive agent shows promise for gastric carcinoma intervention.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Silibinin, a flavonoid, exhibits chemopreventive properties against various cancers.
  • The efficacy of Silibinin in gastric cancer remains underexplored.

Purpose of the Study:

  • To investigate the effects of Silibinin on apoptosis and cell-cycle arrest in human gastric cancer cells (SGC-7901).
  • To elucidate the molecular mechanisms underlying Silibinin's anti-cancer activity.

Main Methods:

  • Human gastric carcinoma SGC-7901 cells were treated with varying doses and durations of Silibinin.
  • Cell growth inhibition, cell-cycle distribution, and apoptosis were assessed.
  • Protein and mRNA levels of key regulatory molecules (p34cdc2, p53, p21, caspases) were analyzed.

Main Results:

  • Silibinin significantly inhibited SGC-7901 cell growth in a dose- and time-dependent manner.
  • Silibinin induced a prominent G2 phase cell-cycle arrest and apoptosis.
  • Mechanistically, Silibinin decreased p34cdc2 protein levels and increased p53 and p21 protein and mRNA levels.
  • Silibinin-induced apoptosis occurred independently of caspase activation.

Conclusions:

  • Silibinin acts as a cell-cycle regulator and apoptosis inducer in human gastric carcinoma SGC-7901 cells.
  • Silibinin demonstrates potential as a chemopreventive agent for gastric carcinoma prevention and intervention.

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