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Functional p53 is required for triptolide-induced apoptosis and AP-1 and nuclear factor-kappaB activation in gastric

X H Jiang1, B C Wong, M C Lin

  • 1Department of Gastroenterology, Rui-jin Hospital, Shanghai, Peoples Republic of China.

Oncogene
|December 26, 2001
PubMed

Insights

Triptolide, derived from Tripterygium wilfordii Hook f, inhibits gastric cancer cell growth and induces apoptosis. Its anti-tumor effects are dependent on a functional p53 protein, highlighting a key mechanism for potential cancer therapies.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Triptolide, a compound from Tripterygium wilfordii Hook f (TWHf), shows promise as an anti-neoplastic agent.
  • Gastric cancer remains a significant health concern, necessitating novel therapeutic strategies.
  • The role of p53 in cancer cell response to natural compounds is an area of active research.

Purpose of the Study:

  • To investigate the therapeutic potential and underlying mechanisms of triptolide against human gastric cancer cells.
  • To determine the influence of p53 status on triptolide's efficacy in gastric cancer.
  • To elucidate triptolide's effects on cell proliferation, apoptosis, and key signaling pathways.

Main Methods:

  • Utilized four human gastric cancer cell lines with varying p53 statuses (wild-type and mutant).
  • Assessed triptolide's impact on cell growth inhibition and apoptosis induction.
  • Investigated effects on NF-kappaB and AP-1 transactivation, p53, p21(waf1/cip1), and bax protein expression, caspase activity, and cell cycle progression.
  • Employed antisense oligonucleotide and dominant-negative p53 to examine p53's role.

Main Results:

  • Triptolide inhibited cell growth and induced apoptosis in gastric cancer cells with wild-type p53 (AGS, MKN-45).
  • Triptolide suppressed NF-kappaB and AP-1 transactivation, upregulated p53, p21(waf1/cip1), and bax, increased caspase activity, and caused G(0)/G(1) cell cycle arrest.
  • Apoptosis induction and NF-kappaB inhibition by triptolide were abrogated upon p53 suppression, confirming p53's essential role.
  • Triptolide showed limited efficacy in gastric cancer cells with mutant p53 (MKN-28, SGC-7901).

Conclusions:

  • Triptolide exhibits anti-tumor and anti-inflammatory effects in gastric cancer cells by inhibiting proliferation and inducing apoptosis.
  • A functional p53 protein is crucial for mediating triptolide's pro-apoptotic, anti-inflammatory, and anti-tumor activities.
  • Triptolide's differential efficacy based on p53 status suggests its potential as a targeted therapy for gastric cancers with functional p53.

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