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

作者信息

Bertova Anna, Kontar Szilvia, Ksinanova Martina, Vergara Alberto Yoldi, Sulova Zdena, Breier Albert, Imrichova Denisa

机构信息

Institute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.

Institute of Biochemistry and Microbiology, Faculty of Chemical and Food Technology, Slovak University of Technology in Bratislava, Radlinského 9, 812 37 Bratislava, Slovakia.

出版信息

Int J Mol Sci. 2024 Dec 17;25(24):13511. doi: 10.3390/ijms252413511.

DOI:10.3390/ijms252413511
PMID:39769273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11677715/
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.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/5f7b1c934479/ijms-25-13511-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/6c7f5423a9a9/ijms-25-13511-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/caca72fe5fda/ijms-25-13511-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/3003f0e3dd33/ijms-25-13511-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/4b55c6b83bb8/ijms-25-13511-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/e24feb5f3b78/ijms-25-13511-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/1a51f4cf0ee4/ijms-25-13511-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/5f7b1c934479/ijms-25-13511-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/6c7f5423a9a9/ijms-25-13511-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/caca72fe5fda/ijms-25-13511-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/3003f0e3dd33/ijms-25-13511-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/4b55c6b83bb8/ijms-25-13511-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/e24feb5f3b78/ijms-25-13511-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/1a51f4cf0ee4/ijms-25-13511-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e551/11677715/5f7b1c934479/ijms-25-13511-g007.jpg

相似文献

[1]
Sulforaphane and Benzyl Isothiocyanate Suppress Cell Proliferation and Trigger Cell Cycle Arrest, Autophagy, and Apoptosis in Human AML Cell Line.

Int J Mol Sci. 2024-12-17

[2]
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Anticancer Res. 2005

[3]
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[4]
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[5]
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Acta Pharmacol Sin. 2017-4

[6]
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J Nutr. 2012-5-30

[7]
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[8]
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[9]
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[10]
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引用本文的文献

[1]
Sulforaphane and Brain Health: From Pathways of Action to Effects on Specific Disorders.

Nutrients. 2025-4-15

本文引用的文献

[1]
Sulforaphane inhibits histone deacetylase causing cell cycle arrest and apoptosis in oral squamous carcinoma cells.

Med J Armed Forces India. 2024

[2]
A Comparative Review of Key Isothiocyanates and Their Health Benefits.

Nutrients. 2024-3-7

[3]
Anti-Leukemic Activity of Brassica-Derived Bioactive Compounds in HL-60 Myeloid Leukemia Cells.

Int J Mol Sci. 2022-11-2

[4]
Plant-Derived Sulforaphane Suppresses Growth and Proliferation of Drug-Sensitive and Drug-Resistant Bladder Cancer Cell Lines In Vitro.

Cancers (Basel). 2022-9-26

[5]
Effects of Sulforaphane-Induced Cell Death upon Repeated Passage of Either P-Glycoprotein-Negative or P-Glycoprotein-Positive L1210 Cell Variants.

Int J Mol Sci. 2022-9-16

[6]
Hormesis: Wound healing and keratinocytes.

Pharmacol Res. 2022-9

[7]
Inhibiting autophagy enhances sulforaphane-induced apoptosis targeting NRF2 in esophageal squamous cell carcinoma.

Acta Pharm Sin B. 2021-5

[8]
Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7.

Int J Mol Sci. 2020-11-18

[9]
The phytoprotective agent sulforaphane prevents inflammatory degenerative diseases and age-related pathologies via Nrf2-mediated hormesis.

Pharmacol Res. 2021-1

[10]
Cell Death Effects Induced by Sulforaphane and Allyl Isothiocyanate on P-Glycoprotein Positive and Negative Variants in L1210 Cells.

Molecules. 2020-4-30

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