Evidence map›Paper›PMID 39769273›Full record

ArticleInternational journal of molecular sciences2024

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

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

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
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  4. Review
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  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Anna BertovaInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.
Szilvia KontarInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.
Martina KsinanovaInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.
Alberto Yoldi VergaraInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.
Zdena SulovaInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.ORCID 0000-0001-7603-4491
Albert BreierInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.ORCID 0000-0003-2174-786X
Denisa ImrichovaInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská Cesta 9, 840 05 Bratislava, Slovakia.

Funding

Grant Agency of the Ministry of Education of the Slovak Republic and the Slovak Academy of Sciences VEGA 2/0130/21Slovak Research and Development Agency APVV-22-0383, APVV-20-0243
6 · The paper itself

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.

Indexed as

ApoptosisAutophagyCell Cycle CheckpointsCell ProliferationIsothiocyanatesLeukemia, Myeloid, AcuteSulfoxidesCell Line, TumorCell SurvivalDrug Resistance, NeoplasmHumansbenzyl isothiocyanateIsothiocyanatessulforaphaneSulfoxidesABCB1 transporterapoptotic proteinsbenzyl isothiocyanate (BITC)cyclin-dependent kinasescyclinsleukemiamultidrug resistancenatural productsulforaphane (SFN)

Identifiers

PMID39769273
PMCPMC11677715

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.