Evidence map›Paper›PMID 21472003›Full record

ArticleCell death & disease2011

Phenethyl isothiocyanate exhibits antileukemic activity in vitro and in vivo by inactivation of Akt and activation of JNK pathways.

N Gao, A Budhraja, S Cheng, E-H Liu, J Chen, Z Yang, D Chen, Z Zhang, X Shi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Article
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  8. Article
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  12. Review
  13. 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
  14. Induction of ApoptosisJournal of cancer prevention · 2019
    Article
  15. Article
  16. Review
  17. Review
  18. Article
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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

9 authors at 4 institutions in 2 countries.

N GaoDepartment of Pharmacognosy, College of Pharmacy, III Military Medical University, Chongqing, China. gaoning59@yahoo.com.cn
A Budhraja
S Cheng
E-H Liu
J Chen
Z Yang
D Chen
Z Zhang
X Shi
Army Medical University · CNUniversity of Kentucky · USSouthwest Hospital · CNThe Graduate Center, CUNY · US

Funding

Apple Peel Extract Protects UV-Induced CarcinogenesisR01ES015375 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2006 to 2010
$1.7M
NIEHS NIH HHS R01 ES015375
6 · The paper itself

Abstract

Effects of phenethyl isothiocyanate (PEITC) have been investigated in human leukemia cells (U937, Jurkat, and HL-60) as well as in primary human acute myeloid leukemia (AML) cells in relation to apoptosis and cell signaling events. Exposure of cells to PEITC resulted in pronounced increase in the activation of caspase-3, -8, -9, cleavage/degradation of PARP, and apoptosis in dose- and time-dependent manners. These events were accompanied by the caspase-independent downregulation of Mcl-1, inactivation of Akt, as well as activation of Jun N-terminal kinase (JNK). Inhibition of PI3K/Akt by LY294002 significantly enhanced PEITC-induced apoptosis. Conversely, enforced activation of Akt by a constitutively active Akt construct markedly abrogated PEITC-mediated JNK activation, Mcl-1 downregulation, caspase activation, and apoptosis, and also interruption of the JNK pathway by pharmacological or genetically (e.g., siRNA) attenuated PEITC-induced apoptosis. Finally, administration of PEITC markedly inhibited tumor growth and induced apoptosis in U937 xenograft model in association with inactivation of Akt, activation of JNK, as well as downregulation of Mcl-1. Taken together, these findings represent a novel mechanism by which agents targeting Akt/JNK/Mcl-1 pathway potentiate PEITC lethality in transformed and primary human leukemia cells and inhibitory activity of tumor growth of U937 xenograft model.

Indexed as

AnimalsAntineoplastic AgentsApoptosisFemaleGene Expression Regulation, LeukemicHL-60 CellsHumansIsothiocyanatesJNK Mitogen-Activated Protein KinasesJurkat CellsLeukemiaMaleMiceMice, SCIDProto-Oncogene Proteins c-aktSignal TransductionAntineoplastic AgentsIsothiocyanatesJNK Mitogen-Activated Protein Kinasesphenethyl isothiocyanateProto-Oncogene Proteins c-akt

Identifiers

PMID21472003
PMCPMC3122055
OpenAlexW2047161358

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.