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Mefenamic acid-induced apoptosis in human liver cancer cell-lines through caspase-3 pathway

Dong Ho Woo1, In-Seob Han, Guhung Jung

  • 1School of Biological Sciences, Seoul National University, 151-742, South Korea.

Life Sciences
|September 8, 2004
PubMed

Insights

Mefenamic acid, a non-steroidal anti-inflammatory drug (NSAID), inhibits liver cancer cell proliferation. This study shows it induces apoptosis in human liver cancer cells via caspase-3 activation.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) exhibit anti-proliferative and apoptosis-inducing properties in various cancer types.
  • Mefenamic acid (MEF) is a non-steroidal anti-inflammatory drug (NSAID) with potential anti-cancer applications.

Purpose of the Study:

  • To investigate the effect of mefenamic acid (MEF) on the proliferation of human liver cancer cells.
  • To elucidate the mechanism by which MEF affects liver cancer cell viability.

Main Methods:

  • Human liver cancer cell lines (Huh-7 and Chang) were treated with mefenamic acid (MEF).
  • Apoptosis was assessed by morphological changes, cell cycle analysis (sub G1 phase), and Annexin V binding.
  • Caspase-3 activity and Poly (ADP-ribose) polymerase 1 (PARP-1) cleavage were measured.
  • The role of caspase-3 was confirmed using a caspase-3 inhibitor.

Main Results:

  • Mefenamic acid (MEF) treatment led to significant apoptotic morphological changes in Huh-7 and Chang cells.
  • A 3-fold and 6-fold increase in sub G1 phase cells was observed in MEF-treated Huh-7 and Chang cells, respectively, at 200 microM.
  • MEF enhanced Annexin V binding, indicating apoptosis, and increased caspase-3 activity.
  • Caspase-3 activation resulted in the cleavage of PARP-1 and caspase-3 itself.
  • Inhibition of caspase-3 blocked PARP-1 cleavage and protected cells from MEF-induced apoptosis.

Conclusions:

  • Mefenamic acid (MEF) effectively inhibits the proliferation of human liver cancer cells.
  • MEF induces apoptosis in liver cancer cells through the activation of the caspase-3 pathway.
  • These findings suggest MEF as a potential therapeutic agent for liver cancer treatment.

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