Evidence map›Paper›PMID 24113589›Full record

ArticleInternational journal of molecular sciences2013

Characterization of apoptosis induced by emodin and related regulatory mechanisms in human neuroblastoma cells.

Fu-Jen Huang, Yan-Der Hsuuw, Wen-Hsiung Chan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Aloe and its Effects on Cancer: A Narrative Literature Review.The East African health research journal · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. EMODIN EFFICACY ON THE AKT, MAPK, ERK AND DNMT EXPRESSION PATTERN DURING DMBA-INDUCED ORAL CARCINOMA IN GOLDEN SYRIAN HAMSTERS.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2016
    Article
  13. Article
  14. 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

3 authors at 3 institutions in 1 country.

Fu-Jen HuangDepartment of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan. whchan@cycu.edu.tw.
Yan-Der Hsuuw
Wen-Hsiung Chan
Chang Gung University · TWChung Yuan Christian University · TWNational Pingtung University of Science and Technology · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emodin (1,3,8-trihydroxy-6-methylanthraquinone), a major constituent of rhubarb, has a wide range of therapeutic applications. Recent studies have shown that emodin can induce or prevent cell apoptosis, although the precise molecular mechanisms underlying these effects are unknown. Experiments from the current study revealed that emodin (10-20 μM) induces apoptotic processes in the human neuroblastoma cell line, IMR-32, but exerts no injury effects at treatment doses below 10 μM. Treatment with emodin at concentrations of 10-20 μM led to a direct increase in the reactive oxygen species (ROS) content in IMR-32 cells, along with significant elevation of cytoplasmic free calcium and nitric oxide (NO) levels, loss of mitochondrial membrane potential (MMP), activation of caspases-9 and -3, and cell death. Pretreatment with nitric oxide (NO) scavengers suppressed the apoptotic biochemical changes induced by 20 μM emodin, and attenuated emodin-induced p53 and p21 expression involved in apoptotic signaling. Our results collectively indicate that emodin at concentrations of 10-20 μM triggers apoptosis of IMR-32 cells via a mechanism involving both ROS and NO. Based on the collective results, we propose a model for an emodin-triggered apoptotic signaling cascade that sequentially involves ROS, Ca²⁺, NO, p53, caspase-9 and caspase-3.

Indexed as

ApoptosisCalciumCaspase 3Caspase 9Cell DeathCell Line, TumorCyclin-Dependent Kinase Inhibitor p21CytoplasmEmodinHumansMembrane Potential, MitochondrialNeuroblastomaNitric OxideReactive Oxygen SpeciesTumor Suppressor Protein p53CalciumCaspase 3Caspase 9Cyclin-Dependent Kinase Inhibitor p21EmodinNitric OxideReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID24113589
PMCPMC3821607
OpenAlexW2055685589

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.