Evidence map›Paper›PMID 24901249›Full record

ArticlePloS one2014

Glabridin mediate caspases activation and induces apoptosis through JNK1/2 and p38 MAPK pathway in human promyelocytic leukemia cells.

Hsin-Lien Huang, Ming-Ju Hsieh, Ming-Hsien Chien, Hui-Yu Chen, Shun-Fa Yang, Pei-Ching Hsiao

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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review on the Diverse Biological Effects of Glabridin.Drug design, development and therapy · 2023
    Review
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  6. Licorice (OncoTargets and therapy · 2022
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  7. Article
  8. Review
  9. Solid-State Fermentation ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Glabridin arrests cell cycle and inhibits proliferation of hepatocellular carcinoma by suppressing braf/MEK signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  18. Article
  19. 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

6 authors at 2 institutions in 1 country.

Hsin-Lien HuangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Ming-Ju HsiehInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Cancer Research Center, Changhua Christian Hospital, Changhua, Taiwan; School of Optometry, Chung Shan Medical University, Taichung, Taiwan.
Ming-Hsien ChienGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Hui-Yu ChenInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Pei-Ching HsiaoSchool of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.
Chung Shan Medical University · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlabridin, a prenylated isoflavonoid of G. glabra L. roots, has been associated with a wide range of biological properties such as regulation of energy metabolism, estrogenic, neuroprotective, anti-osteoporotic, and skin-whitening in previous studies. However, the effect of glabridin on tumor cells metastasis has not been clearly clarified. Here, the molecular mechanism by which glabridin anticancer effects in human promyelocytic leukemia cells was investigated. METHODOLOGY AND PRINCIPAL

findingsThe results showed that glabridin significantly inhibited cell proliferation of four AML cell lines (HL-60, MV4-11, U937, and THP-1). Furthermore, glabridin induced apoptosis of HL-60 cells through caspases-3, -8, and -9 activations and PARP cleavage in dose- and time-dependent manner. Moreover, western blot analysis also showed that glabridin increase phosphorylation of ERK1/2, p38 MAPK and JNK1/2 in dose- and time-dependent manner. Inhibition of p38 MAPK and JNK1/2 by specific inhibitors significantly abolished the glabridin-induced activation of the caspase-3, -8 and -9.

conclusionTaken together, our results suggest that glabridin induced HL-60 cell apoptosis through p38 MAPK and JNK1/2 pathways and could serve as a potential additional chemotherapeutic agent for treating AML.

Indexed as

ApoptosisCaspase 3Caspase 8Caspase 9CaspasesCell Line, TumorCell ProliferationEnzyme ActivationEnzyme InhibitorsHL-60 CellsHumansIsoflavonesLeukemia, Promyelocytic, AcuteMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9p38 Mitogen-Activated Protein KinasesCaspase 3Caspase 8Caspase 9CaspasesEnzyme InhibitorsglabridinIsoflavonesMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9p38 Mitogen-Activated Protein KinasesPhenolsPoly(ADP-ribose) Polymerases

Identifiers

PMID24901249
PMCPMC4047044
OpenAlexW2036864615

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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.