Sulforaphane and Benzyl Isothiocyanate Suppress Cell Proliferation and Trigger Cell Cycle Arrest, Autophagy, and Apoptosis in Human AML Cell Line
2024

Effects of Sulforaphane and Benzyl Isothiocyanate on Human Leukemia Cells

publication 10 minutes Evidence: moderate

Author Information

Author(s): Anna Bertova, Szilvia Kontar, Martina Ksinanova, Alberto Vergara Yoldi, Zdena Sulova, Albert Breier, Denisa Imrichova

Primary Institution: Institute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences

Hypothesis

This study investigates the effects of sulforaphane and benzyl isothiocyanate on cell proliferation, cell death, and drug resistance in human acute myeloid leukemia cells.

Conclusion

Both sulforaphane and benzyl isothiocyanate effectively inhibit the growth of acute myeloid leukemia cells, with benzyl isothiocyanate showing greater potency.

Supporting Evidence

  • Benzyl isothiocyanate was found to be a more potent inhibitor of cell viability than sulforaphane.
  • Both compounds induced apoptosis in the tested leukemia cell lines.
  • Sulforaphane primarily induced cell cycle arrest in the G2/M phase.
  • Benzyl isothiocyanate increased the sub-G1 population, indicative of apoptosis.
  • Both compounds showed significant cytotoxic effects against drug-resistant leukemia cells.

Takeaway

This study found that two natural compounds, sulforaphane and benzyl isothiocyanate, can help stop cancer cells from growing and can even make them die.

Methodology

The study used human acute myeloid leukemia SKM-1 cells and their drug-resistant SKM/VCR variant to assess the effects of sulforaphane and benzyl isothiocyanate on cell viability, apoptosis, and cell cycle progression.

Limitations

The study primarily focuses on in vitro results, which may not fully represent in vivo conditions.

Participant Demographics

The study used human acute myeloid leukemia cell lines derived from a 76-year-old male patient.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.3390/ijms252413511

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