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Sulforaphane and Benzyl Isothiocyanate Suppress Cell Proliferation and Trigger Cell Cycle Arrest, Autophagy, and
Anna Bertova1, Szilvia Kontar1, Martina Ksinanova1
1Institute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.
Abstract:
Isothiocyanates (ITCs) are naturally occurring sulfur-containing compounds with diverse biological effects. This study investigated the effects of sulforaphane (SFN, an aliphatic ITC) and benzyl isothiocyanate (BITC, an aromatic ITC) on human acute myeloid leukemia SKM-1 cells, focusing on cell proliferation, cell death, and drug resistance. Both drug-sensitive SKM-1 cells and their drug-resistant SKM/VCR variant, which overexpresses the drug transporter P-glycoprotein, were used. SFN and BITC reduced cell viability in a dose-dependent manner, with BITC showing greater potency. IC50 values ranged from 7.0-8.0 µM for SFN and 4.0-5.0 µM for BITC in both cell types, with only slight differences between the variants. Both ITCs induced autophagy as evidenced by increased LC3-II production and caused a significant increase in the sub-G0/G1 cell population, especially with BITC. Apoptosis was more pronounced after BITC treatment, whereas SFN had a weaker effect. These results suggest that autophagy may act as a defense mechanism in response to ITC-induced apoptosis in human AML cells.
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