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Induction of caspase-dependent, p53-mediated apoptosis by apigenin in human neuroblastoma

Risa Torkin1, Jean-François Lavoie, David R Kaplan

  • 1Cancer Research Program, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada, M5G 1X8.

Molecular Cancer Therapeutics
|January 20, 2005
PubMed

Insights

Apigenin, a dietary flavonoid, effectively inhibits neuroblastoma growth and induces apoptosis in cancer cells. This compound shows therapeutic potential for neuroblastoma by targeting a p53-Bax-caspase-3 pathway without harming healthy neurons.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Neuroblastoma is a significant cause of childhood cancer mortality, particularly in older children.
  • Existing treatments have limitations, necessitating the search for novel therapeutic agents.
  • Apigenin, a dietary flavonoid, exhibits known antitumor properties in various cancer cell lines.

Purpose of the Study:

  • To investigate the efficacy of apigenin in inhibiting the growth and inducing apoptosis of human neuroblastoma cell lines.
  • To elucidate the molecular mechanisms underlying apigenin's anti-neuroblastoma effects.
  • To assess the therapeutic potential of apigenin for neuroblastoma treatment.

Main Methods:

  • Treatment of neuroblastoma cell lines (NUB-7, LAN-5, SK-N-BE(2)) with apigenin.
  • Assessment of cell viability, colony formation, and apoptosis.
  • Xenograft studies in a mouse model to evaluate in vivo tumor growth inhibition.
  • Analysis of key proteins in apoptosis pathways, including p53, p21WAF1/CIP1, Bax, caspase-3, and PARP.
  • Investigation of the role of p53 and Bcl-X(L) in mediating apigenin's effects.

Main Results:

  • Apigenin significantly inhibited neuroblastoma cell growth, colony formation, and survival.
  • Apigenin induced apoptosis in NUB-7 and LAN-5 cells, with structural features of the flavonoid correlating with its inhibitory potential.
  • In vivo studies demonstrated that apigenin suppressed NUB-7 xenograft tumor growth.
  • Apigenin's mechanism involves upregulation of p53 and its downstream targets, leading to caspase-dependent apoptosis.
  • Apigenin selectively induced apoptosis in neuroblastoma cells with wild-type p53 and did not harm primary sympathetic neurons.

Conclusions:

  • Apigenin demonstrates significant anti-neuroblastoma activity both in vitro and in vivo.
  • The compound's therapeutic effect is mediated through the induction of apoptosis via a p53-Bax-caspase-3 pathway.
  • Apigenin represents a promising candidate for neuroblastoma therapy due to its efficacy and lack of toxicity to normal neuronal cells.

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