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Andrographolide induces apoptosis in B16F-10 melanoma cells by inhibiting NF-κB-mediated bcl-2 activation and

P Pratheeshkumar1, K Sheeja, Girija Kuttan

  • 1Amala Cancer Research Centre, Amala Nagar, Thrissur, Kerala, India.

Immunopharmacology and Immunotoxicology
|June 21, 2011
PubMed

Insights

Andrographolide triggers apoptosis in melanoma cells by upregulating pro-apoptotic genes and downregulating anti-apoptotic genes. This natural compound inhibits key transcription factors, offering a potential cancer treatment strategy.

Area of Science:

  • * Oncology
  • * Molecular Biology
  • * Pharmacology

Background:

  • * Cancer is characterized by uncontrolled cell proliferation and resistance to programmed cell death (apoptosis).
  • * Inducing apoptosis is a key strategy in cancer therapy.
  • * B16F-10 melanoma cells are a common model for studying melanoma progression and treatment.

Purpose of the Study:

  • * To investigate the effect of andrographolide on apoptosis induction in B16F-10 melanoma cells.
  • * To examine andrographolide's regulatory impact on transcription factor activation.
  • * To elucidate the molecular mechanisms underlying andrographolide-induced apoptosis.

Main Methods:

  • * Treatment of B16F-10 melanoma cells with varying concentrations of andrographolide.
  • * Assessment of apoptosis using assays for apoptotic bodies, DNA fragmentation, cell cycle analysis, and TUNEL staining.
  • * Gene expression analysis of pro- and anti-apoptotic markers (p53, Bax, caspase-9, caspase-3, bcl-2).
  • * Investigation of transcription factor activation and nuclear translocation (NF-κB subunits, c-fos, ATF-2, CREB).

Main Results:

  • * Andrographolide induced apoptosis and DNA fragmentation in a dose-dependent manner.
  • * Upregulation of pro-apoptotic genes (p53, Bax, caspase-9, caspase-3) and downregulation of anti-apoptotic gene (bcl-2) were observed.
  • * Andrographolide inhibited the activation and nuclear translocation of NF-κB subunits (p65, p50, c-Rel) and other transcription factors.
  • * Altered production and expression of pro-inflammatory cytokines were noted.

Conclusions:

  • * Andrographolide effectively induces apoptosis in B16F-10 melanoma cells.
  • * The mechanism involves modulating p53-induced pro-apoptotic signaling and inhibiting NF-κB-mediated survival pathways.
  • * Andrographolide demonstrates potential as a therapeutic agent for melanoma by targeting key apoptotic pathways.

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