Evidence map›Paper›PMID 23449451›Full record

ArticleCell death & disease2013

Downregulation of Mcl-1 through inhibition of translation contributes to benzyl isothiocyanate-induced cell cycle arrest and apoptosis in human leukemia cells.

T Zhou, G Li, B Cao, L Liu, Q Cheng, H Kong, C Shan, X Huang, J Chen, N Gao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Review
  3. Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Benzyl isothiocyanate exhibits antibacterial and antibiofilm activity againstFrontiers in cellular and infection microbiology · 2025
    Article
  6. Article
  7. Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Benzyl isothiocyanate inhibits invasion and induces apoptosis via reducing S100A4 expression and increases PUMA expression in oral squamous cell carcinoma cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

10 authors at 2 institutions in 1 country.

T ZhouDepartment of Pharmacognosy, School of Pharmacy, 3rd Military Medical University, Chongqing, China.
G Li
B Cao
L Liu
Q Cheng
H Kong
C Shan
X Huang
J Chen
N Gao
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benzyl isothiocyanate (BITC) is one of the compounds of ITCs' family that has attracted a great deal of interest because of its ability to exhibit anticancer activity. In this study, we investigated the effects of BITC on cell cycle arrest and apoptosis in human leukemia cell lines, primary leukemia cells, and nude mice Jurkat xenograft. Exposure of Jurkat cells to BITC resulted in dose- and time-dependent increase in apoptosis, caspase activation, cytochrome c release, nuclear apoptosis-inducing factor (AIF) accumulation, Bcl2-associated X protein (Bax) translocation, and myeloid cell leukemia-1 (Mcl-1) downregulation. Treatment with these cells also resulted in cell cycle arrest at the G2/M phase. The G2/M-arrested cells are more sensitive to undergoing Mcl-1 downregulation and apoptosis mediated by BITC. BITC downregulates Mcl-1 expression through inhibition of translation, rather than through a transcriptional, post-translational, or caspase-dependent mechanism. Dephosphorylation of eukaryotic initiation factor 4G could contribute to the inhibition of Mcl-1 translation mediated by BITC. Furthermore, ectopic expression of Mcl-1 substantially attenuates BITC-mediated lethality in these cells, whereas knockdown of Mcl-1 through small interfering RNA significantly enhances BITC-mediated lethality. Finally, administration of BITC markedly inhibited tumor growth and induced apoptosis in Jurkat xenograft model in association with the downregulation of Mcl-1. Taken together, these findings represent a novel mechanism by which agents targeting Mcl-1 potentiate BITC lethality in transformed and primary human leukemia cells and inhibitory activity of tumor growth of Jurkat xenograft model.

Indexed as

AnimalsApoptosisApoptosis Inducing Factorbcl-2-Associated X ProteinDown-RegulationEukaryotic Initiation Factor-4GG2 Phase Cell Cycle CheckpointsHL-60 CellsHumansIsothiocyanatesJurkat CellsLeukemiaMiceMice, NudeM Phase Cell Cycle CheckpointsMyeloid Cell Leukemia Sequence 1 ProteinApoptosis Inducing Factorbcl-2-Associated X Proteinbenzyl isothiocyanateEukaryotic Initiation Factor-4GIsothiocyanatesMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID23449451
PMCPMC3734843
OpenAlexW2001018121

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.