Evidence map›Paper›PMID 25144448›Full record

ArticlePloS one2014

Pterostilbene simultaneously induced G0/G1-phase arrest and MAPK-mediated mitochondrial-derived apoptosis in human acute myeloid leukemia cell lines.

Pei-Ching Hsiao, Ying-Erh Chou, Peng Tan, Wei-Jiunn Lee, Shun-Fa Yang, Jyh-Ming Chow, Hui-Yu Chen, Chien-Huang Lin, Liang-Ming Lee, Ming-Hsien Chien

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Review
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  7. Article
  8. The Anti-Leukemic Activity of Natural Compounds.Molecules (Basel, Switzerland) · 2021
    Review
  9. Article
  10. Article
  11. Anti-Stem Cell Property of Pterostilbene in Gastrointestinal Cancer Cells.International journal of molecular sciences · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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  19. Oncotarget · 2017
    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 4 institutions in 1 country.

Pei-Ching HsiaoSchool of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.
Ying-Erh ChouInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Peng TanGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.
Wei-Jiunn LeeDepartment of Urology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Jyh-Ming ChowDepartment of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Hui-Yu ChenInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Chien-Huang LinGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
Liang-Ming LeeDepartment of Urology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Ming-Hsien ChienGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan; Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Chung Shan Medical University · TWTaipei Medical University · TWWan Fang Hospital · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPterostilbene (PTER) is a dimethylated analog of the phenolic phytoalexin, resveratrol, with higher anticancer activity in various tumors. Herein, the molecular mechanisms by which PTER exerts its anticancer effects against acute myeloid leukemia (AML) cells were investigated. METHODOLOGY AND PRINCIPAL

findingsResults showed that PTER suppressed cell proliferation in various AML cell lines. PTER-induced G0/G1-phase arrest occurred when expressions of cyclin D3 and cyclin-dependent kinase (CDK)2/6 were inhibited. PTER-induced cell apoptosis occurred through activation of caspases-8-9/-3, and a mitochondrial membrane permeabilization (MMP)-dependent pathway. Moreover, treatment of HL-60 cells with PTER induced sustained activation of extracellular signal-regulated kinase (ERK)1/2 and c-Jun N-terminal kinase (JNK)1/2, and inhibition of both MAPKs by their specific inhibitors significantly abolished the PTER-induced activation of caspases-8/-9/-3. Of note, PTER-induced cell growth inhibition was only partially reversed by the caspase-3-specific inhibitor, Z-DEVE-FMK, suggesting that this compound may also act through a caspase-independent pathway. Interestingly, we also found that PTER promoted disruption of lysosomal membrane permeabilization (LMP) and release of activated cathepsin B.

conclusionTaken together, our results suggest that PTER induced HL-60 cell death via MAPKs-mediated mitochondria apoptosis pathway and loss of LMP might be another cause for cell apoptosis induced by PTER.

Indexed as

ApoptosisCaspasesCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationEnzyme ActivationExtracellular Signal-Regulated MAP KinasesHL-60 CellsHumansIntracellular MembranesJNK Mitogen-Activated Protein KinasesLeukemia, Myeloid, AcuteLysosomesMatrix MetalloproteinasesMitochondriaCaspasesCell Cycle ProteinsExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesMatrix MetalloproteinasesMitogen-Activated Protein KinasespterostilbeneStilbenes

Identifiers

PMID25144448
PMCPMC4140770
OpenAlexW2078612337

What OpenQuestion 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 OpenQuestion graph.