Apoptosis Induction by Menadione in Human Promyelocytic Leukemia HL-60 Cells

Duck-Jin Sa1, Eun-Jee Lee1, Byung-Sun Yoo1

  • 1Present Address: Department of Life Science, Kyonggi University, Suwon, 443-760 Korea.

Toxicological Research
|February 11, 2020
PubMed

Insights

Menadione (vitamin K-3) induces distinct cell death types in leukemia cells. Low doses trigger apoptosis, while high doses cause necrosis, impacting cell viability and caspase-3 activation.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Oncology

Background:

  • Menadione (vitamin K-3) is a synthetic compound with known biological activities.
  • Understanding its effects on cancer cells is crucial for potential therapeutic applications.

Purpose of the Study:

  • To investigate the mechanisms of cell death induced by menadione in human promyelocytic leukemia HL-60 cells.
  • To differentiate between apoptosis and necrosis pathways triggered by varying menadione concentrations.

Main Methods:

  • HL-60 cells were treated with different concentrations of menadione.
  • Apoptosis and necrosis were assessed using DNA gel electrophoresis and flow cytometry.
  • Caspase-3 activity and poly(ADP-ribose) polymerase (PARP) cleavage were analyzed.

Main Results:

  • Low menadione concentrations (1-50 µM) induced apoptosis, characterized by DNA laddering.
  • High menadione concentration (100 µM) induced necrosis, shown by DNA smearing and reduced cell viability.
  • Menadione activated caspase-3, with peak activity at 50 µM, but low activity at 100 µM.

Conclusions:

  • Menadione induces mixed cell death modalities in HL-60 cells.
  • Concentration-dependent effects dictate whether apoptosis or necrosis occurs.
  • The findings provide insights into menadione's cytotoxic mechanisms in leukemia.

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