Evidence map›Paper›PMID 27376261›Full record

ArticleMolecules (Basel, Switzerland)2016

18α-Glycyrrhetinic Acid Induces Apoptosis of HL-60 Human Leukemia Cells through Caspases- and Mitochondria-Dependent Signaling Pathways.

Yi-Chang Huang, Chao-Lin Kuo, Kung-Wen Lu, Jen-Jyh Lin, Jiun-Long Yang, Rick Sai-Chuen Wu, Ping-Ping Wu, Jing-Gung Chung

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.0field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

  1. A novel bakuchiol aminoguanidine derivative induces apoptosis in human triple-negative breast cancer cells.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
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  7. Concurrent production of glycyrrhetic acid 3-Bioresources and bioprocessing · 2021
    Article
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  9. Article
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  11. Review
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  15. 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

8 authors at 2 institutions in 1 country.

Yi-Chang HuangDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan. YCH@mail.cmu.edu.tw.
Chao-Lin KuoDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 404, Taiwan. clkuo@mail.cmu.edu.tw.
Kung-Wen LuCollege of Chinese Medicine, School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 404, Taiwan. prorna@mail.cmu.edu.tw.
Jen-Jyh LinDivision of Cardiology, China Medical University Hospital, Taichung 404, Taiwan. pig222@ms15.hinet.net.
Jiun-Long YangDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 404, Taiwan. JLY@mail.cmu.edu.tw.
Rick Sai-Chuen WuDepartment of Anesthesiology, China Medical University Hospital, Taichung 404, Taiwan. rickwu@mail.cmuh.org.tw.
Ping-Ping WuSchool of Pharmacy, China Medical University, Taichung 404, Taiwan. ppwu@mail.cmu.edu.tw.
Jing-Gung ChungDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan. jgchung@mail.cmu.edu.tw.
China Medical University · TWAsia University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study we investigate the molecular mechanisms of caspases and mitochondria in the extrinsic and intrinsic signal apoptosis pathways in human leukemia HL-60 cells after in vitro exposure to 18α-glycyrrhetinic acid (18α-GA). Cells were exposed to 18α-GA at various concentrations for various time periods and were harvested for flow cytometry total viable cell and apoptotic cell death measurements. Cells treated with 18α-GA significantly inhibited cell proliferation and induced cell apoptosis in a dose-dependent manner, with an IC50 value of 100 μM at 48 h. The cell growth inhibition resulted in induction of apoptosis and decreased the mitochondria membrane potential (ΔΨm) and increased caspase-8, -9 and -3 activities. Furthermore, cytochrome c and AIF were released from mitochondria, as shown by western blotting and confirmed by confocal laser microscopy. Western blotting showed that 18α-GA increased the levels of pro-apoptotic proteins such as Bax and Bid and decreased the anti-apoptotic proteins such as Bcl-2 and Bcl-xl, furthermore, results also showed that 18α-GA increased Fas and Fas-L which are associated with surface death receptor in HL-60 cells. Based on those observations, the present study supports the hypothesis that 18α-GA-induced apoptosis in HL-60 cells involves the activation of the both extrinsic and intrinsic apoptotic pathways.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsCaspasesCell ProliferationDNA DamageGene ExpressionGlycyrrhetinic AcidHL-60 CellsHumansMembrane Potential, MitochondrialMitochondriaProtein TransportSignal Transduction18alpha-glycyrrhetinic acidAntineoplastic AgentsApoptosis Regulatory ProteinsCaspasesGlycyrrhetinic Acid18α-glycyrrhetinic acidapoptosiscaspase-3HL-60 cellsmitochondria

Identifiers

PMID27376261
PMCPMC6273602
OpenAlexW2468138006

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.